PReD-Bench/PRed-Bench huggingface dataset:
Mahanimbine Exerts Anticancer Effects on Human Pancreatic Cancer Cells by Triggering Cell Cycle Arrest, Apoptosis, and Modulation of AKT/Mammalian Target of Rapamycin (mTOR) and Signal Transducer and Activator of Transcription 3 (STAT3) Signalling Pathways
Authors: Xuejun Gong
Shuai Liang
Chenlin Pei
Qun He
Journal: Medical Science Monitor (2018)
Discipline: CLINICAL MEDICINE
Keywords: Pancreatic cancer; Mahanimbine; Anticancer potential; Cell proliferation; Apoptosis
Affiliations: Department of Obstetrics, Xiangya Hospital, Central South University, Changsha, Hunan, China (mainland)., Department of Pancreatic Biliary Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China (mainland).

Abstract:  BACKGROUND Pancreatic cancer causes tremendous mortality across the globe mainly due to late diagnosis and unavailability of efficient chemotheruptic agents. In the current study the anticancer potential of a plant derived alkaloid, Mahanimbine, was examined against a panel of pancreatic cancer cells. MATERIAL AND METHODS The cell proliferation was determined by MTT assay. Annexin V/PI and DAPI staining were performed to detect apoptosis. Cell cycle distribution was investigated by flow cytometery. Cell migration was detected by wound healing assay and protein expression was checked by western blotting. RESULTS The results revealed that Mahanimbine could inhibit the proliferation of the all the pancreatic cancer cells with lower cytoxicity against the normal cells. The IC50 ranged from 3.5 to 64 µM against the pancreatic cancer cell lines. The lowest IC50 of 3.5 µM was observed tor the Capan-2 and SW119 pancreatic cancer cell lines. The anticancer activity of Mahanimbine against the Capan-2 and SW119 cells was found to be due to G0/G1 cell cycle arrest and induction of apoptosis. Mahanimbine prompted apoptosis was also associated with decline in Bcl-2 and enhancement of the Bax expression. Further, it was observed that Mahanimbine could inhibit the AKT/mTOR and STAT3 signalling pathways in the Capan-2 and SW119 pancreatic cancer cells. The effects of the Mahanimbine were also examined on the migration of the Capan-2 and SW119 pancreatic cancer cells. It was found that Mahanimbine could inhibit the motility and migration of both the pancreatic cancer cell lines. CONCLUSIONS We found that Mahanimbine inhibits the proliferation of pancreatic cancer cells and as such Mahanimbine may prove beneficial in the management of pancreatic cancer. 

Retracted: No

PubPeer comments:
 *[left]* Figure 8 from [Pei et al (2018)] .  Effect of Mahanimbine on the migration of migration of Capan-2 and SW1190 cells, as depicted by wound healing assay . *[right]* Figure 5 from [Zhang et al (2018)] .  Rosmarinic acid treatment led to the suppression of the cancer cell migration in OVCAR-3 cancer cells. The cells were treated with 0, 40 and 160 u00b5M dose of rosmarinic acid for 48 hrs. Unexpected overlaps. ![file] ,
Honokiol, a phytochemical from Magnolia spp., inhibits breast cancer cell migration by targeting nitric oxide and cyclooxygenase-2
Authors: Tripti Singh
Santosh K Katiyar
Journal: International Journal of Oncology (2011)
Discipline: CLINICAL MEDICINE
Keywords: honokiol; cancer cell migration; breast cancer; nitric oxide; cGMP
Affiliations: Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

Abstract:  In the present study, we report the effects of honokiol, a phytochemical from Magnolia spp., on cancer cell migration capacity and the molecular mechanisms underlying these effects using breast cancer cell lines as an in vitro model. Using cell migration assays, we found that the treatment of human breast cancer cells (MCF-7) and murine mammary cancer cells (4T1) with honokiol resulted in a dose-dependent inhibition of migration of these cells, which was associated with a reduction in nitric oxide (NO) levels. The cell migration capacity was decreased in the presence of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase. Honokiol reduced the elevated levels of cyclic guanosine monophosphate (cGMP) in the cells, while the treatment of 4T1 cells with guanylate cyclase (GC) inhibitor 1-H-[1,2,4]oxadiaxolo[4,3-a]quinolalin-1-one (ODQ) reduced the migration of cells and the levels of cGMP. The presence of 8-bromoguanosine 3'5'-cyclic monophosphate, an analogue of cGMP, enhanced the migration of these cells, suggesting a role for GC in the migration of 4T1 cells. Honokiol also inhibited the levels of cyclooxygenase-2 (COX-2) and prostaglandin (PG) E2 in 4T1 cells. The transfection of 4T1 cells with COX-2 siRNA resulted in a reduction in cell migration. ODQ and L-NAME also decreased the levels of PGE2 in 4T1 cells suggesting a role for COX-2/PGE2 in cell migration. Moreover, honokiol inhibited the activation of nuclear factor κB (NF-κB), an upstream regulator of COX-2 and iNOS, in 4T1 cells. These results indicate that NO and COX-2 are the key targets of honokiol in the inhibition of breast cancer cell migration, an essential step in invasion and metastasis. 

Retracted: No

PubPeer comments:
 Identified by another reader. See also: https: www.the-scientist.com daily-news scientist-who-received-millions-from-nih-leaves-alabama-posts-36659 *** ![file] ,
C4b-binding protein (C4BP) activates B cells through the CD40 receptor
Authors: Federica Angelini
Emiko Mizoguchi
Hiroshi Fujiwara
Scott R Brodeur
Luigi D Notarangelo
Alessandro Plebani
Bjorn Dahlback
Leonard B Bacharier
Erdyni Tsitsikov
Raif S Geha
Anna M Blom
Journal: Immunity (2003)
Discipline: IMMUNOLOGY
Keywords: C4BP; CD40; B cells; proliferation; CD54
Affiliations: Division of Immunology, Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA, USA.

Abstract:  We demonstrate that the alpha chain of human C4b binding protein (C4BP) binds directly to CD40 on human B cells at a site that differs from that used by CD40 ligand. C4BP induces proliferation, upregulation of CD54 and CD86 expression, and IL4-dependent IgE isotype switching in normal B cells but not in B cells from patients with CD40 or IKKgamma/NEMO deficiencies. Furthermore, C4BP colocalized with B cells in the germinal centers of human tonsils. These observations suggest that C4BP is an activating ligand for CD40 and establish a novel interface between complement and B cell activation. 

Retracted: No

PubPeer comments:
 Figure 7A. Much more similar than expected. ![file] ,
Long non-coding RNA BLACAT1 inhibits prostate cancer cell proliferation through sponging miR-361
Authors: H-Y Li
F-Q Jiang
L Chu
X Wei
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: LncRNAs; BLACAT1; prostate cancer; miR-361; proliferation
Affiliations: Department of Urology, China-Japan Union Hospital of Jilin University, Changchun, People's Republic of China. .

Abstract:  Objective: LncRNAs play a key role in the development and progression of prostate cancer. In this study, the effects of the lncRNA BLACAT1 in prostate cancer were investigated. Patients and methods: Real-time PCR was used to detect the expression of BLACAT1 and miR-361 in prostate cancer tissues and adjacent normal tissues (n=25). The function of BLACAT1 was detected through proliferation assay and apoptosis assay. The interaction between BLACAT1 and miR-361 in prostate cancer was studied by luciferase assay, RNA immunoprecipitation assay and chromatin immunoprecipitation analysis were performed to detect the BLACAT1 binding proteins. The xenograft mice experiment was performed to further confirm the functional significance of lncRNA BLACAT1 in vivo. Results: In patient samples and prostate cancer cell lines, BLACAT1 was down-regulated and inversely proportional to DNMT1, HDAC1, EZH2, MDM2 and miR-361 expression. Treatment with 5-azacytidine and chidamide enhanced BLACAT1 expression and decreased the levels of miR-361. The BALCAT1 promoter was methylated in prostate cancer tissue and found to interact with miR-361 via luciferase assays. BLACAT1 bound to EZH2, DNMT1 and HDAC1. ChIP-seq analysis revealed that HDAC1 interacts with STAT3, while EZH2 interacts with the mitogen-activated protein kinase (MAPK) promoter. Conclusions: Two regulatory axes of BLACAT1-EZH2-MAPK and BLACAT1-HDAC1-STAT3 were identified to be associated with the progression of prostate cancer. Both chidamide and 5-azacytidine represent promising therapeutic options in prostate cancer treatment. 

Retracted: No

PubPeer comments:
 Figure 4C and 4D. It seems to be an error in the process of making the figure. ![file] , 
 Actually, in addition, Bax in 4C appears to be rotated 180 degrees from Bax in 4D. The other panels also share similarities between 4C and 4D. , 
 Dear Parashorea Tomentella and Gregariella Coarctata: I am sorry for the late replies because I did not get any information about your comments before. Thank you for your comments to our article, regarding to these Western blot pics in 4C and 4D. After carefully checking, we noticed that we might have made some mistakes when we generated the figures. We have contacted other authors and will email the editors to correct the errors. I apologize for any confusion this may have caused to you and other readers. We will try to fix it ASAP. ,
Benzyl Isothiocyanate Inhibits Prostate Cancer Development in the Transgenic Adenocarcinoma Mouse Prostate (TRAMP) Model, Which Is Associated with the Induction of Cell Cycle G1 Arrest
Authors: Gyoo Taik Kwon
Zunnan Huang
Do Young Lim
Ki Won Lee
Han Jin Cho
Young-Hee Kang
Hyerim Song
Zigang Dong
Yoon Sin Oh
Ji Hee Kim
Jung Han Yoon Park
Journal: International Journal of Molecular Sciences (2016)
Discipline: CHEMISTRY
Keywords: TRAMP; benzyl isothiocyanate; cell cycle arrest; prostate cancer development.
Affiliations: Department of Food Science and Nutrition, Hallym University, Chuncheon 200-702, Korea. ., WCU Biomodulation Major, Department of Agricultural Biotechnology and Center for Food and Bioconvergence, Seoul National University, Seoul 151-921, Korea. ., The Hormel Institute, University of Minnesota, Austin, MN 55912, USA. ., Advanced Institutes of Convergence Technology, Seoul National University, Suwon 443-270, Korea. ., Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Dongguan Scientific Research Center, Guangdong Medical University, Dongguan, Guangdong 523808, China. ., Department of Molecular Medicine, School of Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-799, Korea. ., Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 151-742, Korea. .

Abstract:  Benzyl isothiocyanate (BITC) is a hydrolysis product of glucotropaeolin, a compound found in cruciferous vegetables, and has been shown to have anti-tumor properties. In the present study, we investigated whether BITC inhibits the development of prostate cancer in the transgenic adenocarcinoma mouse prostate (TRAMP) mice. Five-week old, male TRAMP mice and their nontransgenic littermates were gavage-fed with 0, 5, or 10 mg/kg of BITC every day for 19 weeks. The weight of the genitourinary tract increased markedly in TRAMP mice and this increase was suppressed significantly by BITC feeding. H and E staining of the dorsolateral lobes of the prostate demonstrated that well-differentiated carcinoma (WDC) was a predominant feature in the TRAMP mice. The number of lobes with WDC was reduced by BITC feeding while that of lobes with prostatic intraepithelial neoplasia was increased. BITC feeding reduced the number of cells expressing Ki67 (a proliferation marker), cyclin A, cyclin D1, and cyclin-dependent kinase (CDK)2 in the prostatic tissue. In vitro cell culture results revealed that BITC decreased DNA synthesis, as well as CDK2 and CDK4 activity in TRAMP-C2 mouse prostate cancer cells. These results indicate that inhibition of cell cycle progression contributes to the inhibition of prostate cancer development in TRAMP mice treated with BITC. 

Retracted: No

PubPeer comments:
 Figure 2A appears to have three sets of repeated images. *** ![file] ,
The major genetic risk factor for severe COVID-19 is inherited from Neanderthals
Authors: Hugo Zeberg
Svante Pääbo
Journal: Nature (2020)
Discipline: Multidisciplinary
Keywords: genetic association study; chromosome 3; respiratory failure; severe acute respiratory syndrome coronavirus 2; SARS-CoV-2
Affiliations: Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany. ., Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. ., Okinawa Institute of Science and Technology, Onna-son, Japan. .

Abstract:  A recent genetic association study1 identified a gene cluster on chromosome 3 as a risk locus for respiratory failure after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A separate study (COVID-19 Host Genetics Initiative)2 comprising 3,199 hospitalized patients with coronavirus disease 2019 (COVID-19) and control individuals showed that this cluster is the major genetic risk factor for severe symptoms after SARS-CoV-2 infection and hospitalization. Here we show that the risk is conferred by a genomic segment of around 50 kilobases in size that is inherited from Neanderthals and is carried by around 50% of people in south Asia and around 16% of people in Europe. 

Retracted: No

PubPeer comments:
 This paper is discussing an interesting theory that certain genes located at chromosome 3 leads to increased risk of severe outcome of Covid-19. In light of this theory, it is interesting to compare the vulnernability of Covid-19 in immigrants to Scandinavia. Immigrants from Somalia and Ethiopia show the similar increased vulnerability as people from Pakistan. However, they don t express the mentioned  genetic risk factor linked to chromosome 3. Furthermore, immigrants from India,which do have the inherited Neanderthals genetics, do not show the same vulnerability compared to immigrants from Pakistan. The vulnerability to Covid-19 in certain immigrant populations has also been explained by sosio-economical factors, generally poor health and traveling exposure to high infection pressure in their home countries. ,
Regulation of alpha1 Na/K-ATPase expression by cholesterol
Authors: Qiqi Ye
Zijian Xie
Yiliang Chen
Runming Jing
Xin Li
Jiang Tian
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Na/K-ATPase; cholesterol; caveolin-1; plasma membrane; Src kinase
Affiliations: Department of Physiology and Pharmacology, College of Medicine, University of Toledo, Toledo, Ohio 43614-2598, USA.

Abstract:  We have reported that α1 Na/K-ATPase regulates the trafficking of caveolin-1 and consequently alters cholesterol distribution in the plasma membrane. Here, we report the reciprocal regulation of α1 Na/K-ATPase by cholesterol. Acute exposure of LLC-PK1 cells to methyl β-cyclodextrin led to parallel decreases in cellular cholesterol and the expression of α1 Na/K-ATPase. Cholesterol repletion fully reversed the effect of methyl β-cyclodextrin. Moreover, inhibition of intracellular cholesterol trafficking to the plasma membrane by compound U18666A had the same effect on α1 Na/K-ATPase. Similarly, the expression of α1, but not α2 and α3, Na/K-ATPase was significantly reduced in the target organs of Niemann-Pick type C mice where the intracellular cholesterol trafficking is blocked. Mechanistically, decreases in the plasma membrane cholesterol activated Src kinase and stimulated the endocytosis and degradation of α1 Na/K-ATPase through Src- and ubiquitination-dependent pathways. Thus, the new findings, taken together with what we have already reported, revealed a previously unrecognized feed-forward mechanism by which cells can utilize the Src-dependent interplay among Na/K-ATPase, caveolin-1, and cholesterol to effectively alter the structure and function of the plasma membrane. 

Retracted: No

PubPeer comments:
 FIG 6B Different organs have the same result ![file] ,
Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a
Authors: Tongguo Qiu
Chao Qi
David M Ricketts
Shouyun Zhang
Changhui Li
Yuanji Wang
Journal: Cancer Biology & Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: NNT-AS1; long noncoding RNA; miR-320a; osteosarcoma.
Affiliations: a Department of Orthopedics , People's Hospital of Rizhao , Shandong , China., b Department of medicine , Kuishan branch of People's Hospital of Rizhao , Shandong , China., c Department of Orthopedics , Brighton and Sussex University Hospitals , UK., d Department of Orthopedics , Affiliated Hospital of Qingdao University , Shandong , China.

Abstract:  Objective: To investigate the role and mechanism of action of nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) in osteosarcoma (OS). Methods: Bioinformatic analysis suggested miR-320a as potential target of NNT-AS1. Influence of NNT-AS1 overexpression or knockdown on OS cell proliferation, colony-formation, apoptosis, migration and invasion capacity was first investigated. Expression levels of NNT-AS1, miR-320a, beta-catenin, RUNX2, IGF-1R, c-Myc, Cyclin D1 and MMP13 were also evaluated by RT-qPCR and western blotting accordingly. Xenograft models using U2OS and OS-732 cells with different NNT-AS1 gene modifications were constructed for tumor formation assay as well as evaluation of miR-320a, beta-catenin and RUNX2 expression in primary lesion. NNT-AS1-overexpressing U2OS cells and NNT-AS1-knockdown OS-732 cells were subject to miR-320a mimic and inhibitor transfection, respectively, to investigate the miR-320a dependency of the osteosarcoma-promoting role of NNT-AS1. Results: NNT-AS1 overexpression significantly increased proliferation, survival and mobility of U2OS cells in vitro as well as its tumor formation ability in vivo, while NNT-AS1 knockdown showed opposite effect on OS-732 cells. In both in vitro and in vivo model, NNT-AS1 expression level significantly correlated with that of beta-catenin, RUNX2, IGF-1R, c-Myc, Cyclin D1 and MMP13 as well as Akt phosphorylation level, and inversely correlated with miR-320a expression. Transfection of miR-320a mimic significantly inhibiter the promoting effect of NNT-AS1 on cell proliferation, survival and mobility of U2OS cells, while miR-320 inhibitor partially rescued that of OS-732 cells. Conclusion: NNT-As1 functions as a cancer-promoting lncRNA by downregulating miR-320a, thus increasing the protein expression level of beta-catenin, RUNX2 and IGF-1R as well as activation of Akt in osteosarcoma. 

Retracted: No

PubPeer comments:
 Figure 2G and figure 4I appear to entirely overlap, though their images are for different cell lines and treatments... ![file] ![file] ,
Tumor-suppressive function and mechanism of HOXB13 in right-sided colon cancer
Authors: Yiming Lv
Binbin Xie
Xing Gao
Ying Lou
Yuzi Xu
Zhipeng Fang
Hongming Pan
Yunlong Liu
Fei Wu
Bingjun Bai
Weidong Han
Journal: Signal transduction and targeted therapy (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Tumour biomarkers.
Affiliations: 1Department of Medical Oncology; Sir Run Run Shaw Hospital; School of Medicine, Zhejiang University, Hangzhou, 310016 PR China., 2Department of Colorectal Surgery; Sir Run Run Shaw Hospital; School of Medicine, Zhejiang University, Hangzhou, 310016 PR China., 3Department of Stomatology; Stomatology Hospital; School of Medicine, Zhejiang University, Hangzhou, 310000 PR China., 4Department of Medical Oncology; The Second Affiliated Hospital of Suzhou University; School of Medicine, Suzhou University, Suzhou, 215000 PR China., 5School of Medicine, Anhui University of Science and Technology, Huainan, 232001 PR China.

Abstract:  Right-sided colon cancer (RCC) and left-sided colon cancer (LCC) differ in their clinical and molecular features. An investigation of differentially expressed genes (DEGs) between RCC and LCC could contribute to targeted therapy for colon cancer, especially RCC, which has a poor prognosis. Here, we identified HOXB13, which was significantly less expressed in RCC than in LCC and associated with prognosis in RCC, by using 5 datasets from the Gene Expression Omnibus (GEO). Tissue sample analysis showed that HOXB13 was differentially expressed between normal and only RCC tumor tissues. HOXB13 inhibited colon cancer cell proliferation and induced apoptosis both in vitro and in vivo. Furthermore, we found that HOXB13 might be regulated by DNMT3B and suppress C-myc expression to exert antitumor effects via β-catenin/TCF4 signals in RCC. In conclusion, the current study is the first to demonstrate that HOXB13 has a tumor-suppressive effect in RCC. High expression levels of HOXB13 are associated with prolonged overall survival in patients with RCC. The DNMT3B-HOXB13-C-myc signaling axis might be a molecular target for the treatment of RCC. 

Retracted: No

PubPeer comments:
 Brought to my attention by a reader. * Red boxes: Two b-actin panels in Supplementary Figure 8 (A and C) look more similar than expected. ![file] , 
 Thank you for your inquiry. We will seriously investigate and deal with it as soon as possible. , 
 #1 We carefully checked the original data of the experiment and found that there were indeed some errors in processing figures. We are deeply sorry for this. We confirmed that these errors did not influence the statistical analysis, the overall results and conclusions of this article. We have contacted the editorial department to correct this problem. Thank you for your query. ,
LncRNA-MALAT1 influences myocardial infarction by regulating miR-30a/beclin-1 pathway
Authors: J Zhang
J-F He
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA-MALAT1; miR-30a; BECN1; myocardial infarction; rats
Affiliations: Department of Emergency, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China. .

Abstract:  Objective: Long non-coding ribonucleic acid-metastasis-associated lung adenocarcinoma transcript 1 (lncRNA-MALAT1) has been confirmed as a key factor involving in various physiological and pathological processes. The present study aims to investigate whether lncRNA-MALAT1 affects the process of myocardial infarction (MI) in rats by regulating the micro RNA (miR-30a)/Beclin-1 (BECN1) pathway. Materials and methods: Twelve healthy male Sprague-Dawley rats were randomly selected and equally divided into sham-operation group and MI group. In MI group, a rat model of acute MI (AMI) was established by ligating the left anterior descending coronary artery. Rats in sham-operation group were set as the control. The messenger RNA (mRNA) expression levels of lncRNA-MALAT1, miR-30a, and BECN1 in the infarcted myocardial tissues were detected via real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). The rat myocardial cell line H9c2 was cultured in vitro and then transfected with vectors of lncRNA-MALAT1, miR-30a, and BECN1. After that, qRT-PCR was performed to measure mRNA levels of lncRNA-MALAT1, miR-30a, and BECN1 in H9c2 cells. The protein level of BECN1 in cells was determined via Western blotting (WB) assay. Results: Expression levels of lncRNA-MALAT1 and BECN1 in the rat myocardium of MI group were up-regulated markedly (p&lt;0.01), while miR-30a was down-regulated notably (p&lt;0.01) compared with those in sham-operation group. After H9c2 cells were transfected with overexpression vectors of lncRNA-MALAT1 or miR-30a, expression levels of miR-30a (p&lt;0.01) and BECN1 (p&lt;0.01) were remarkably down-regulated, respectively. Conclusions: LncRNA-MALAT1 up-regulates the expression of BECN1 by binding to miR-30a, thereby increasing the level of cell autophagy after MI. 

Retracted: No

PubPeer comments:
 ![file] Fig6: same loading control: GAPDH, although different samples: overexpressed Malat1 versus knocked-down Malat1. ,
Control of stress-dependent cardiac growth and gene expression by a microRNA
Authors: Lillian B Sutherland
Eva van Rooij
James A Richardson
Eric N Olson
Xiaoxia Qi
Joseph Hill
Journal: Science (2007)
Discipline: Multidisciplinary
Keywords: heart; stress; hypertrophic growth; fibrosis; contractility
Affiliations: Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.

Abstract:  The heart responds to diverse forms of stress by hypertrophic growth accompanied by fibrosis and eventual diminution of contractility, which results from down-regulation of alpha-myosin heavy chain (alphaMHC) and up-regulation of betaMHC, the primary contractile proteins of the heart. We found that a cardiac-specific microRNA (miR-208) encoded by an intron of the alphaMHC gene is required for cardiomyocyte hypertrophy, fibrosis, and expression of betaMHC in response to stress and hypothyroidism. Thus, the alphaMHC gene, in addition to encoding a major cardiac contractile protein, regulates cardiac growth and gene expression in response to stress and hormonal signaling through miR-208. 

Retracted: No

PubPeer comments:
 Figure 1. * Red boxes and arrows: The U6 panels from the  Normal and  Failing subjects appear to look similar, albeit in mirrored orientation. ![file] ,
The efficacy of Labetalol versus Nitroglycerin for induction of controlled hypotension during sinus endoscopic surgery. A prospective, double-blind and randomized study
Authors: Nagat S El-Shmaa
Ahmed Younes
Hoda Alsaid Ahmed Ezz
Journal: Journal of Clinical Anesthesia (2017)
Discipline: CLINICAL MEDICINE
Keywords: Controlled hypotension; Labetalol; Nitroglycerin; Sinus endoscopic surgery.
Affiliations: Department of Anesthesia & Surgical ICU, Faculty of Medicine, Tanta University, Egypt., Department of ENT, Faculty of Medicine, Tanta University, Egypt. Electronic address: .

Abstract:  Objective: To assess the efficacy of labetalol versus nitroglycerin for induction of controlled hypotension during sinus endoscopic surgery. Design: A prospective, double-blind and randomized study. Setting: Carried out in operating room in university hospital. Patients: 60 patients of both sexes, American Society of Anesthesiologists (ASA) physical status I and II, age range from 20 to 60years; scheduled for elective sinus endoscopic surgery under general anesthesia (GA). Interventions: Patients were divided into two groups (30 each). NTG group received nitroglycerin infusion at a dose of 2-5μg/kg/min, LAB group received labetalol infusion at a dose of 0.5-2mg/min. Measurements: Surgical condition was assessed by surgeon using average category scale (ACS) of 0-5, a value of 2-3 being ideal. In both groups mean arterial blood pressure (MAP) was gradually reduced till the ideal ACS for assessment of surgical condition, the target of ACS was 2-3 or lower. Results: Both studied drugs achieved desired hypotension and improved visualization of surgical field by decreasing bleeding in the surgical site, but ideal surgical conditions were created at mild hypotension (MAP 70-75) in LAB group while same conditions were created at MAP of 65-69mmHg in NTG group. Mean heart rate (HR) was significantly higher in NTG group as compared to LAB group. Blood loss decreased significantly in LAB group. Conclusion: Both labetalol and NTG are effective and safe drugs for induction of controlled hypotension during sinus endoscopic surgery. While, labetalol was better as it offered optimum operative condition with mild decrease in blood pressure, decreased surgical bleeding and less tachycardia during the surgery. 

Retracted: No

PubPeer comments:
 I wonder if the authors of this paper can clarify how the demographic data for the two groups are identical to that for two of the three groups in an entirely different study previously published by the same authors in the same journal... 10.1016 j.jclinane.2016.01.037 ![file] ![file] In the earlier paper C=control, A=dexmedetomidine and B=labetalol. In the later paper, NTG=nitroglycerin and LAB=labetalol. ,
LncRNA LINC00460 promotes the papillary thyroid cancer progression by regulating the LINC00460/miR-485-5p/Raf1 axis
Authors: Guangjun Li
Qingli Kong
Journal: Biological research (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: LINC00460; Papillary thyroid cancer; Progression; Raf1; miR-485-5p.
Affiliations: Department of Oncology, Yuncheng County Hospital of Traditional Chinese Medicine, Heze, 274700, Shandong, China., Department of Oncology, The Affiliated Hospital of Jining Medical University, No. 89, Gutun Road, Jining, 272029, Shandong, China. .

Abstract:  Background: Papillary thyroid cancer (PTC) is the most common malignancy of all thyroid cancers. LncRNA LINC00460 has been proved to play roles in the oncogenesis and progression of various tumors, including papillary thyroid cancer. However, the potential molecular mechanism of LINC00460 in PTC is poorly investigated. Results: LINC00460 was upregulated in PTC tissues and cells. Raf1 was upregulated in PTC tissues, but miR-485-5p was down-regulated. High LINC00460 expression was associated with poor prognosis. LINC00460 knockdown suppressed proliferation, migration, invation and EMT of PTC cells. Bioinformatics prediction revealed that LINC00460 had binding sites with miR-485-5p, which was validated by luciferase reporter assay. In addition, miR-485-5p was confirmed to directly target Raf1 3'-UTR. Moreover, LINC00460 promoted PTC progression by sponging miR-485-5p to elevate the expression of Raf1. Knockdown of LINC00460 restrained tumor growth in vivo. Conclusion: LINC00460 induced proliferation, migration, invation and EMT of PTC cells by regulating the LINC00460/miR-485-5p/Raf1 axis, which indicated that LINC00460 may be a potential biomarker and therapeutic target for PTC. 

Retracted: No

PubPeer comments:
 Figure S2 is a duplicate of Figure 3 from this 2014 Sci Rep article , 
 A correction was issued: https: pubs.acs.org doi 10.1021 jacs.0c06670 ,
Pyramid-Shaped PEG-PCL-PEG Polymeric-Based Model Systems for Site-Specific Drug Delivery of Vancomycin with Enhance Antibacterial Efficacy
Authors: Arshid Numan
Majed M Alrobaian
Prashant Kesharwani
Nagashekhara Molugulu
Sima Singh
Nikhil Agrawal
Journal: ACS Omega (2020)
Discipline: CHEMISTRY
Keywords: Antibacterial resistance; drug delivery; vancomycin; PEG; PCL
Affiliations: Discipline of Pharmaceutical Sciences, College of Health Sciences, University of KwaZulu-Natal, Private Bag X54001, Durban 4000, South Africa, Department of Pharmaceutics and Industrial Pharmacy, College of Pharmacy, Taif University, Taif 21974, Kingdom of Saudi Arabia, School of Pharmacy, Monash University, Jalan Lagoon Selatan, Bandar Sunway 47500, Selangor, Malaysia, State Key Laboratory of ASIC and System, SIST, Fudan University, 200433 Shanghai, China, Department of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, 110062 New Delhi, India

Abstract:  Antibacterial resistance remains a major global problem due to frequent prescriptions, leading to significant toxicities. To overcome the limitations of antibiotic therapy, it is highly desirable to provide site-specific delivery of drugs with controlled release. Inspired by the biocompatible, biodegradable, and site-specific mimicking behavior of poly(ethylene glycol) (PEG) and poly(caprolactone) (PCL), we developed vancomycin-PEG-PCL-PEG conjugates to maximize the pharmacological effects and minimize the side effects. Drug-loaded vancomycin-PEG-PCL-PEG conjugates are influenced by size, shape, surface area, encapsulation efficiency, in vitro drug release, hemolysis assay, cytotoxicity, and antibacterial activity against methicillin-resistant Staphylococcus aureus (MRSA) and bacterial kill kinetics. The results demonstrated that vancomycin (VCM) release from PEG-PCL-PEG triblock revealed a biphasic manner. Hemolysis assay showed the nonprescription nature of VCM-PEG-PCL-PEG. Cytotoxicity studies confirmed the biocompatibility of VCM-PEG-PCL-PEG. The in vitro antibacterial results showed enhance activity with minimum inhibitory concentration compared to bare VCM. Molecular dynamics simulation study revealed that binding between VCM and PEG-PCL-PEG by hydrophobic interactions offers molecular encapsulation and steric barrier to drug degradation. This newly developed therapeutic delivery system can offer to enhance activity and delivery VCM against MRSA. 

Retracted: No

PubPeer comments:
 Figure 4. Panel B and C both FITR spectra are the same for different chemical compounds. Panel B spectra color was changed, shortened to produce Panel C. Could authors clarify on the duplication of the graph. ![file] ,
Proliferation-associated Brn-3b transcription factor can activate cyclin D1 expression in neuroblastoma and breast cancer cells
Authors: S Bowen
D S Latchman
L Samady
S Irshad
V S Budhram-Mahadeo
S A Lee
G P Tonini
Journal: Oncogene (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Brn-3b; proliferation; neuroblastoma; breast cancer; tumour growth
Affiliations: Medical Molecular Biology Unit, Institute of Child Health, University College London, London, UK. 

Abstract:  Brn-3b transcription factor enhances proliferation of neuroblastoma (NB) and breast cancer cell lines in vitro and increases the rate and size of in vivo tumour growth, whereas reducing Brn-3b slows growth, both in vitro and in vivo. Brn-3b is elevated in &gt;65% of breast cancer biopsies, and here we demonstrate that Brn-3b is also elevated in NB tumours. We show a significant correlation between Brn-3b and cyclin D1 (CD1) in breast cancers and NB tumours and cell lines. Brn-3b directly transactivates the CD1 promoter in co-transfection experiments, whereas electrophoretic mobility shift assay and chromatin immunoprecipitation assays demonstrate that Brn-3b protein binds to an octamer sequence located in the proximal CD1 promoter. Site-directed mutagenesis of this sequence resulted in loss of transactivation of the CD1 promoter by Brn-3b. Thus, Brn-3b may act to alter growth properties of breast cancer and NB cells by enhancing CD1 expression in these cells. 

Retracted: No

PubPeer comments:
null, 
null, 
 https: www.the-scientist.com ?articles.view articleNo 54605 title Chief-Academic-Officer-Accused-in-Ongoing-Research-Scandal-at-UCL  Two scientists, Anastasis Stephanou and Tiziano Scarabelli, were found to have doctored images in seven papers on which Latchman was a co-author. I do not see the names of Anastasis Stephanou, or Tiziano Scarabelli, as authors on this paper. , 
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null, 
 https: www.theguardian.com science 2019 jul 01 research-misconduct-claim-upheld-against-former-head-of-ucl-lab https: www.buzzfeednews.com article peteraldhous david-latchman-scientific-misconduct ,
LncRNA HOTAIR contributes to the malignancy of hepatocellular carcinoma by enhancing epithelial-mesenchymal transition via sponging miR-23b-3p from ZEB1
Authors: Kai Tan
An Chen
Tao Yang
Xiaojun He
Xilin Du
Journal: Gene (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Epithelial-mesenchymal transition; HOTAIR; Hepatocellular carcinoma; ZEB1; miR-23b-3p.
Affiliations: Department of General Surgery, Tangdu Hospital, the Fourth Military Medical University, Shaanxi 710038, Xi'an, China., Department of General Surgery, Tangdu Hospital, the Fourth Military Medical University, Shaanxi 710038, Xi'an, China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). Several figures presented in the manuscript appear to have been doctored. Figure 2B copied areas from figure 2C in the publication Gene 675 (2018) 102-109 https://doi.org/10.1016/j.gene.2018.06.095 At higher contrast, the western blots in Figures 2F, 4F, and 4J show signs of image manipulation. The journal has tried to contact the authors of this article. As there is no explanation for the image manipulations, the Editors-in-Chief of Gene have lost confidence in the validity of this work and have decided to retract it. 

Retracted: Yes

PubPeer comments:
 Fig. 3A and B might contain a duplication. Could the authors check please? ![file] A similar possible duplication can be spotted when you compare Fig. 3B with Fig. 5D ![file] , 
 Figure 5D. Could the authors confirm that the images selected represent the treatment groups properly? *** Brightness adjusted ![file] ,
Liver-specific deletion of the growth hormone receptor reveals essential role of growth hormone signaling in hepatic lipid metabolism
Authors: Derek Le Roith
Yong Fan
Mark A Sperling
David Hwang
Massimo Trucco
John J Kopchick
Ram K Menon
Pinchas Cohen
Douglas J DiGirolamo
Thomas Clemens
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Growth hormone; Insulin-like growth factor I; Liver; GHRLD; Bone density
Affiliations: Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260, USA.

Abstract:  Growth hormone (GH) plays a pivotal role in growth and metabolism, with growth promotion mostly attributed to generation of insulin-like growth factor I (IGF-I) in liver or at local sites of GH action, whereas the metabolic effects of GH are considered to be intrinsic to GH itself. To distinguish the effects of GH from those of IGF-I, we developed a Cre-lox-mediated model of tissue-specific deletion of the growth hormone receptor (GHR). Near total deletion of the GHR in liver (GHRLD) had no effect on total body or bone linear growth despite a &gt;90% suppression of circulating IGF-I; however, total bone density was significantly reduced. Circulating GH was increased 4-fold, and GHRLD displayed insulin resistance, glucose intolerance, and increased circulating free fatty acids. Livers displayed marked steatosis, the result of increased triglyceride synthesis and decreased efflux; reconstitution of hepatic GHR signaling via adenoviral expression of GHR restored triglyceride output to normal, whereas IGF-I infusion did not correct steatosis despite restoration of circulating GH to normal. Thus, with near total absence of circulating IGF-I, GH action at the growth plate, directly and via locally generated IGF-I, can regulate bone growth, but at the expense of diabetogenic, lipolytic, and hepatosteatotic consequences. Our results indicate that IGF-I is essential for bone mineral density, whereas hepatic GH signaling is essential to regulate intrahepatic lipid metabolism. We propose that circulating IGF-I serves to amplify the growth-promoting effects of GH, while simultaneously dampening the catabolic effects of GH. 

Retracted: No

PubPeer comments:
 There are undeclared cut and splice sites in Figure 2B (red arrow). Could authors show the original gel data at here? ![file] ,
BNIP1 inhibits cell proliferation, migration and invasion, and promotes apoptosis by mTOR in cervical cancer cells
Authors: W-F Yu
L Ran
S Zhou
M Chen
Z Huang
L Xiang
F-H Li
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: BNIP1; cervical cancer; mTOR signaling pathway; proliferation; apoptosis
Affiliations: Department of Oncology, the Second Affiliated Hospital of Soochow University, Suzhou, China. .

Abstract:  Objective: BNIP1, a member of the BH3-only protein family, plays essential roles in a variety of biological processes. However, the mechanism and function of BNIP1 are still unknown in cervical cancer. We aim to explore the roles of BNIP1 on cervical cancer cell proliferation, apoptosis, migration, and invasion abilities by mTOR signaling pathway. Patients and methods: qRT-PCR and Western blot assays were performed to assess BNIP, mTOR, and p70S6K1 expressions. CCK-8, transwell and flow cytometry assays were used to measure the representative proliferation, migration, invasion, and apoptosis abilities. Results: Our findings indicated that BNIP1 is down-expressed in cervical cancer tissues and cells, and was negatively associated with lymphatic metastasis. Overexpression of BNIP1 suppressed proliferation, migration and invasion, and promoted apoptosis of cervical cancer cells. Silence of BNIP1 by siRNAs accelerated proliferation, migration and invasion, and inhibited apoptosis of cervical cancer cells. In addition, we found that BNIP1 significantly inhibited mTOR, p70S6K1, and p-p70S6K1 expressions; BNIP1 affected the proliferation, apoptosis, migration, and invasion abilities of cervical cancer cells by regulating mTOR expression. Conclusions: BNIP1 can be considered a marker for cervical carcinoma therapy. 

Retracted: No

PubPeer comments:
 Figure 2A: * Orange boxes: The BNIP1 Migration and Invasion panels appear to show an area of overlap. * Flow cytometry panels: these panels display a squarish uniform distribution that does not look like any other flow cytometry experiment I have seen before. Could the authors please clarify? ![file] ,
IL-17 contributes to cardiac fibrosis following experimental autoimmune myocarditis by a PKCβ/Erk1/2/NF-κB-dependent signaling pathway
Authors: Zhaoliang Su
Jingping Yin
Huaxi Xu
Shengjun Wang
Zhijun Jiao
Haitao Zhu
Caixia Sun
Siamak Sandoghchian
Hongyan Yuan
Yanfang Liu
Journal: International Immunology (2012)
Discipline: IMMUNOLOGY
Keywords: Myocarditis; dilated cardiomyopathy; T(h)17 cells; IL-17; autoimmune myocarditis
Affiliations: Department of Immunology, Center of Clinical Medicine and Laboratory, Jiangsu University, Zhenjiang 212013, China.

Abstract:  Myocarditis is a common clinical cardiovascular disease, and some patients progress to dilated cardiomyopathy (DCM) with chronic heart failure. Common viral infections are the most frequent cause of myocarditis, but other pathogens and autoimmune diseases have also been implicated. T(h)17 cells are novel IL-17-producing effector T helper cells that play an important role in the development of autoimmune myocarditis. Furthermore, IL-17 is also important in post-myocarditis cardiac remodeling and progression to DCM. However, the mechanisms whereby IL-17 and IL-17-producing cells promote the progression of cardiac fibrosis remain unclear. We therefore investigated whether IL-17 directly induced cardiac fibrosis in experimental autoimmune myocarditis (EAM) and explored the possible molecular mechanisms. The EAM model was induced and serum IL-17 level was detected by ELISA; western blot, immunofluorescence and sirius red staining were used to analyze the collagen expression. PCR was used to assay the IL-17RA and IL-17RC. The results indicated that IL-17 induced cardiac fibrosis both in vitro and in vivo. The protein kinase C (PKC)β/Erk1/2/NF-κB (Nuclear Factor κappa B) pathway was involved in the development of myocardial fibrosis and IL-17 contributed to cardiac fibrosis following EAM via this pathway. These results provide the first direct evidence for the involvement of the PKCβ/Erk1/2/NF-κB signaling pathway in IL-17-induced myocardial fibrosis. 

Retracted: No

PubPeer comments:
 Figure 2F. * Orange boxes: The collagen 1 control panel looks unexpectedly similar to the collagen III 72h panel. ![file] , 
 Figure 2C. * Blue boxes: The left and right b-actin panels look very similar but they represent different time points. ![file] , 
 #2 Dear Elisabeth The time point is marked wrong. Both should be 72h, You can see this from the statistical chart below the western blot; in addition, collagen I III is indeed detected on the same membrane, so the internal control is the same. We will apply to the magazine for correction. Regarding question 1, we are further checking the original data, if it is indeed wrong, we also apply for correction. ![file] ,
Circ_0001658 promotes the proliferation and metastasis of osteosarcoma cells via regulating miR‐382‐5p/YB‐1 axis
Authors: Bo Zhao
Xiujun Su
Pengbin Wang
Lisong Wang
Journal: Cell Biochemistry and Function (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: YB-1; circ_0001658; miR-382-5p; osteosarcoma.
Affiliations: Department of Orthopaedics, Shangluo Central Hospital, Shangluo, Shanxi Province, China.

Abstract:  Circular RNA (circRNA) can modulate the gene expression via sponging microRNA (miRNA) in multiple malignancies. Nevertheless, the detailed function of circ_0001658 in osteosarcoma (OS) and its regulatory mechanism remain elusive. Real-time PCR was carried out to detect the expressions of circ_0001658, miR-382-5p, and Y box-binding protein 1 (YB-1) mRNA in OS tissues. Besides, western blot was done to monitor YB-1 expression in OS cells. Chi-squared test was used to analyse the correlation between circ_0001658 and clinicopathologic characteristics of OS patients. CCK8 assay, colony formation assay, flow cytometry, and transwell assay were performed to determine the function of circ_0001658. Moreover, dual-luciferase reporter gene assay was done to verify the targeting relationship between circ_0001658 and miR-382-5p. Compared with adjacent tissues, circ_0001658 displayed a significantly higher expression in OS tissues. Circ_0001658 could facilitate the proliferation, migration, and invasion of OS cells and impede apoptosis by sponging miR-382-5p. Further, circ_0001658 was proved to directly and negatively regulate the expression of miR-382-5 while positively modulate the expression of YB-1. Circ_0001658 promotes the proliferation and metastasis of OS cells via modulating miR-382-5p/YB-1 axis. SIGNIFICANCE OF THE STUDY: In recent years, the expression and function of circular RNA in cancer have been the focus of tumour research. The study on circular RNA helps elucidate the molecular pathology of tumorigenesis and cancer progression. This study demonstrated that circ_0001658 promotes the proliferation and metastasis of OS cells via modulating miR-382-5p/YB-1 axis. To our best knowledge, this work is the first to study the expression and function of circ_0001658 in cancer. 

Retracted: No

PubPeer comments:
 Figure 3. * Red boxes: The  circ migration and  circ invasion panels look unexpectedly similar. ![file] ,
Protective effect of exogenous hydrogen sulfide on pulmonary artery endothelial cells by suppressing endoplasmic reticulum stress in a rat model of chronic obstructive pulmonary disease
Authors: Da-Wen Wu
Jun-Ying Chen
Qing-Shi Chen
Kai-Xiong Liu
Hai-Bo Ding
Jie-Feng Huang
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Apoptosis; Chronic obstructive pulmonary disease; Endoplasmic reticulum stress; Exogenous hydrogen sulfide; Pulmonary artery endothelial cells.
Affiliations: Division of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian Province, PR China. Electronic address: ., Division of Respiratory and Critical Care Medicine, First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian Province, PR China., Central Lab, First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, Fujian Province, PR China.

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. An Expression of Concern for this article was previously published while an investigation was conducted (see related editorial: https://doi.org/10.1016/j.biopha.2022.113812). This retraction notice supersedes the Expression of Concern published earlier. Concern was raised about the reliability of the Western blot data in Figure 4A, which appear to represent a distinct phenotype as found in many other publications, as detailed here: https://pubpeer.com/publications/029A84E50BD071A2088140723E3CF0; and here: https://docs.google.com/spreadsheets/d/1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY/edit#gid=262337249. Independent analysis confirmed the presence of suspected image duplications between the Western blots in Figure 4A and those contained in Yan et al (2017). The journal requested the corresponding author comment on these concerns and provide the associated raw data. The authors did not respond to this request and therefore the Editor-in-Chief decided to retract the article. 

Retracted: No

PubPeer comments:
 Fig 4A.  determination of protein expression of caspase-12, CHOP and GRP78 in lung tissues in the Control NaHS COPD COPD+NaHS groups by western blot analysis. ![file] These protein blobs come from a restricted gamut. See e.g. Figs 2C, 4C, 10D from [Yan et al (2017)] , especially the loading controls: ![] Or the loading control from 7B of [Zhou et al (2018)] . ![] Their stylised nature is suggestive of a papermill provenance. Other examples are tabulated in a spreadsheet. https: docs.google.com spreadsheets d 1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY edit?usp=sharing ,