PReD-Bench/PRed-Bench huggingface dataset:
Targeting FoxM1 inhibits proliferation, invasion and migration of nasopharyngeal carcinoma through the epithelial‑to-mesenchymal transition pathway
Authors: Hongyan Chen
Chao Yu
Yanan Liu
Taoyu Wen
Lei Wei
Lin Yie
Lili Chen
Journal: Oncology reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: FoxM1; nasopharyngeal carcinoma; migration; invasion; metastasis
Affiliations: Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, P.R. China.

Abstract:  High expression levels of the forkhead box M1 (FoxM1) transcription factor are associated with metastasis and poor prognosis of malignancies. However, little is known concerning its function in nasopharyngeal carcinoma (NPC). The present study aimed to investigate the impact of FoxM1 inhibition on the migration and invasion of NPC cells and the potential mechanisms. The effects of FoxM1 inhibitor treatment and FoxM1 silencing on the proliferation, migration and invasion of NPC CNE-1 and CNE-2 cells were examined by CCK-8, Transwell migration/invasion and colony formation assays. The effects of stable FoxM1 silencing on the growth and lung metastasis of implanted NPC were evaluated. The relative levels of FoxM1, zinc finger E-box binding homeobox 2 (ZEB2), Snail2 and E-cadherin in the different groups of NPC cells and tumors were determined by quantitative real-time PCR, western blotting and immunohistochemical assays. Treatment with thiostrepton, FoxM1 inhibitor, significantly reduced the survival of NPC cells. Treatment with thiostrepton and/or knockdown of FoxM1 inhibited the anchorage-independent proliferation, migration and invasion of NPC cells. Inhibition of FoxM1 also increased the relative levels of E-cadherin, but reduced ZEB2 and Snail2 expression in NPC cells. Stable FoxM1 silencing inhibited the growth and lung metastasis of implanted NPC in vivo, which was associated with increased levels of E-cadherin, but decreased ZEB2 and Snail2 expression in the NPC tumors. In conclusion, our data clearly indicate that knockdown of FoxM1 inhibited the growth and metastasis of human NPC by modulating epithelial-to-mesenchymal transition (EMT), and FoxM1 may be a potential target for the intervention of NPC. 

Retracted: No

PubPeer comments:
 Figure 2 appears to have some image overlaps ![file] ,
Activation of AMP-activated protein kinase by kainic acid mediates brain-derived neurotrophic factor expression through a NF-kappaB dependent mechanism in C6 glioma cells
Authors: Young Taek Oh
Wonchae Choe
Jung Yeon Lee
Ji Hyun Choi
Kyung-Sik Yoon
Joohun Ha
Sung Soo Kim
Insug Kang
Hana Yoon
Hyung Hwan Baik
Ju Hie Lee
Journal: Biochemical and Biophysical Research Communications (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: AMP-activated protein kinase; energy homeostasis; Kainic acid; brain-derived neurotrophic factor; C6 glioma cells
Affiliations: Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.

Abstract:  AMP-activated protein kinase (AMPK) is a key regulator of energy homeostasis. Kainic acid (KA), a prototype excitotoxin is known to induce brain-derived neurotrophic factor (BDNF) in brain. In this study, we examined the role of AMPK in KA-induced BDNF expression in C6 glioma cells. We showed that KA and KA receptor agonist induced activation of AMPK and KA-induced AMPK activation was blocked by inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase (CaMKK) beta. We then showed that inhibition of AMPK by compound C, a selective inhibitor of AMPK, or small interfering RNA of AMPKalpha1 blocked KA-induced BDNF mRNA and protein expression. Inhibition of AMPK blocked KA-induced phosphorylation of CaMKII and I kappaB kinase (IKK) in C6 cells. Finally, we showed that inhibition of AMPK reduced DNA binding and transcriptional activation of nuclear factor-kappaB (NF-kappaB) in KA-treated cells. These results suggest that AMPK mediates KA-induced BDNF expression by regulating NF-kappaB activation. 

Retracted: No

PubPeer comments:
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Side-by-side comparison of the biological characteristics of human umbilical cord and adipose tissue-derived mesenchymal stem cells
Authors: Luyang Du
Li Hu
Niya Gong
Chao Yang
Lili Chen
Jiajia Zhao
Jingqiong Hu
Abhilasha Khanal
Weixiang Ouyang
Jiarong Liu
Journal: BioMed Research International (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Adipose tissue-derived mesenchymal stem cells; Umbilical cord-derived mesenchymal stem cells; Comparative study; Cell surface markers; Adipogenesis
Affiliations: Department of Stomatology, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China., Stem Cell Center, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China, Department of Stomatology, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, Hubei 430022, China, Department of Gynaecology and Obstetrics, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China

Abstract:  Both human adipose tissue-derived mesenchymal stem cells (ASCs) and umbilical cord-derived mesenchymal stem cells (UC-MSCs) have been explored as attractive mesenchymal stem cells (MSCs) sources, but very few parallel comparative studies of these two cell types have been made. We designed a side-by-side comparative study by isolating MSCs from the adipose tissue and umbilical cords from mothers delivering full-term babies and thus compared the various biological aspects of ASCs and UC-MSCs derived from the same individual, in one study. Both types of cells expressed cell surface markers characteristic of MSCs. ASCs and UC-MSCs both could be efficiently induced into adipocytes, osteoblasts, and neuronal phenotypes. While there were no significant differences in their osteogenic differentiation, the adipogenesis of ASCs was more prominent and efficient than UC-MSCs. In the meanwhile, ASCs responded better to neuronal induction methods, exhibiting the higher differentiation rate in a relatively shorter time. In addition, UC-MSCs exhibited a more prominent secretion profile of cytokines than ASCs. These results indicate that although ASCs and UC-MSCs share considerable similarities in their immunological phenotype and pluripotentiality, certain biological differences do exist, which might have different implications for future cell-based therapy. 

Retracted: Yes

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Antagonist of microRNA-21 improves balloon injury-induced rat iliac artery remodeling by regulating proliferation and apoptosis of adventitial fibroblasts and myofibroblasts
Authors: Ming-Xiang Zhang
Xiao-Yang Hou
Pei-Li Bu
Zhi-Hao Wang
Xue-Qiang Zhao
Rong Liu
Fei Wang
Xiu-Ling Wang
Fei Gao
Jun-Ni Liu
Yun Zhang
Journal: Journal of Cellular Biochemistry (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Molecular pathways; adventitial fibroblasts; myofibroblasts; proliferation; apoptosis

Abstract:  Molecular pathways involved in adventitial fibroblasts (AFs) and myofibroblasts (MFs) proliferation and apoptosis contribute to vascular remodeling. MicroRNA-21 (miR-21) plays an important role in regulating cellular proliferation and apoptosis of many cell types; however, the effect of miR-21 on AFs and MFs is still unknown. In this study, we found that miR-21 was expressed in AFs and overexpressed in MFs. Inhibition of miR-21 decreased proliferation and increased apoptosis of AFs and MFs, and overexpression of miR-21 with pre-miR-21 had the reverse effect. Programmed cell death 4 (PDCD4), related to cell proliferation and apoptosis, was validated as a direct target of miR-21 by dual-luciferase reporter assay and gain and loss of function of miR-21 in AFs and MFs. PDCD4 knockdown with siRNA partly rescued the reduced proliferation with miR-21 inhibition and alleviated the increased apoptosis induced by miR-21 inhibition in AFs and MFs. Moreover, increasing PDCD4 expression by miR-21 inhibition significantly decreased JNK/c-Jun activity. In contrast, decreasing PDCD4 expression by pre-miR-21 treatment increased JNK/c-Jun activity, while the effect of miR-21 inhibition on JNK/c-Jun activity could be rescued by PDCD4 siRNA. Moreover, miR-21 inhibition could regulate proliferation and apoptosis of vascular AFs and MFs in vivo. Furthermore, miR-21 inhibition reversed vascular remodeling induced by balloon injury. In summary, our findings demonstrate that miR-21 may have a critical role in regulating proliferation and apoptosis of AFs and MFs, and PDCD4 is a functional target gene involved in the miR-21-mediated cellular effects in vascular remodeling by a miR-21/PDCD4/JNK/c-Jun pathway. 

Retracted: No

PubPeer comments:
  Fig. 7. Antagonist of miR-21 regulated proliferation and apoptosis of AFs and MFs in injured artery. ...(B) TUNEL stainning of uninjured, vehicle-treated and miR-21 antagomirtreated groups. TUNEL-positive cells were stained black-brown. (Scale bars: 50 mm). ![file] Possibly an error in figure assembly. ,
Oncoprotein Bmi-1 renders apoptotic resistance to glioma cells through activation of the IKK-nuclear factor-kappaB Pathway
Authors: Jueheng Wu
Mian He
Li-Yun Gong
Jie Yuan
Li-Ping Liu
Mengfeng Li
Jun Li
Jun-Chao Cai
Lan Wang
Musheng Zeng
Li-Li Jiang
Shi-Yuan Cheng
Li-Bing Song
Journal: American Journal Of Pathology (2010)
Discipline: CLINICAL MEDICINE
Keywords: malignant gliomas; Bmi-1; apoptosis; NF-kappaB; resistance
Affiliations: Departments of Biochemistry, Zhongshan School of Medicine, Sun Yat-Sen University, 74 Zhongshan Road II, Guangzhou, Guangdong 510080, China.

Abstract:  One of the features of malignant gliomas is their deviant resistance to cellular apoptosis induced by cytotoxic reagents. Bmi-1, an oncoprotein, has been linked to oncogenesis and cancer progression in various types of human cancers including gliomas. However, the mechanisms underlying Bmi-1 antiapoptotic function remain largely unknown. In this study, we report that Bmi-1 renders apoptotic resistance to glioma cells through nuclear factor-kappaB (NF-kappaB). In glioma cells, ectopic expression of Bmi-1 significantly inhibits doxorubicin-, BCNU-, or UV irradiation- induced apoptosis through reduction of activated caspase-3 and PARP, and induction of Bcl-X(L). Cellular depletion of Bmi-1 enhances the sensitivity of glioma cells to apoptosis induced by doxorubicin, BCNU, or UV irradiation. Bmi-1 activates NF-kappaB through stimulation of IkappaB phosphorylation, nuclear translocation, and transcriptional activity of NF-kappaB and expression of downstream genes of NF-kappaB including caspase-3, PARP, Bcl-X(L), and c-Myc. Inhibition of the IKK-NF-kappaB pathway abrogates the antiapoptotic effect of Bmi-1 on glioma cells. In high-grade gliomas, Bmi-1 and NF-kappaB are co-expressed in the cell nucleus. Up-regulation of Bmi-1 also correlates with tumor progression and poor survival of patients with gliomas. Together, our data demonstrate that Bmi-1 bestows apoptotic resistance to glioma cells through the IKK-NF-kappaB pathway and suggest Bmi-1 as a useful indicator for glioma prognosis. 

Retracted: No

PubPeer comments:
 Fig. 2B contains two images which appear to overlap. ![file] , 
 Dear Sir or Madam, The authors are very sorry for the careless mistake during figure assembly of Figure 2B. After carefully checking our original data, we found that some images of U251MG treated with UV were saved into the file folder for images of U251MG treated with Doxorubicin, resulting in that representative photograph of cell morphology of cultured U251MG cells treated with Doxorubicin duplicated that of cultured U251MG cells treated with UV (40J M2). We recently have repeated the data and consistently found that overexpressing Bmi-1 potently promotes resistance to UV- or Doxorubicin-induced apoptosis. The authors also wish to state that after our careful re-evaluation and confirmation of all the data in our study, the oversight has no bearing on the conclusions of our original article. We are currently in the process of making the correction and apologize for our mistake again and highly appreciate for your helpful comment. Sincerely, The authors ,
Resistance of hepatocellular carcinoma to sorafenib can be overcome with co-delivery of PI3K/mTOR inhibitor BEZ235 and sorafenib in nanoparticles
Authors: Xueke Liu
Yong Liang
Huaiyong Gan
Shuping Zhou
Binquan Wu
Xiaolong Tang
Yinci Zhang
Shiyu Cai
Amin Li
Journal: Expert Opinion on Drug Delivery (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: BEZ235; Hepatocellular carcinoma; PI3K/mTOR; apoptosis; nanoparticles
Affiliations: Department of Hepatobiliary Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, China, Biochemistry Department, Medical School, Anhui University of Science & Technology, Huainan, China, Central Laboratory, Huai’an Hospital Affiliated of Xuzhou Medical College and Huai’an Second Hospital, Huai’an, P. R. China

Abstract:  Background: The combination of BEZ235 with sorafenib (SFB) enhances anti-hepatocellular carcinoma (HCC) efficacy of the two agents. However, pharmacokinetic profiles in vivo and different endocytosis abilities of these two drugs hinder their therapeutic application.Research design and methods: In this work, we developed d-α-tocopheryl polyethylene glycol 1000 succinate - polycaprolactone polymer nanoparticles (NPs) for co-delivery of SFB and BEZ235 (SFB/BEZ235-NPs). Explored the anti-proliferative and pro-apoptotic effects of SFB/BEZ235-NPs through in vitro and in vivo experiments.Results: Stabilized SFB/BEZ235-NPs were prepared with optimized drug ratio, yielding high encapsulation efficiency, low polydispersity, and enhanced cellular internalization in HepG2 cells. Synergistic cytotoxicity and pro-apoptotic ability were documented. In vivo pharmacokinetic results revealed extended circulation and bioavailability of SFB/BEZ235-NPs compared with those of free drugs. SFB/BEZ235-NPs enhanced antitumor effectiveness in SFB-resistant HCC xenograft mouse models.Conclusion: Taken together, the results of this study describe a promising strategy using SFB and BEZ235 in a nanoparticle formulation for treatment of SFB-resistant HCC. 

Retracted: No

PubPeer comments:
 Figure 7C. https: imgur.com z9Q2Y7v , 
 Figure 6D. https: imgur.com vP52SCk ,
Caveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in Cardiomyocytes
Authors: Alexis M Keefe
Ravi C Balijepalli
Yogananda S Markandeya
Timothy A Hacker
Marites T Woon
Benjamin K August
David M Roth
Hemal H Patel
Laura J Phelan
Courtney R Reynolds
Journal: Journal of Biological Chemistry (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: angiotensin II; calcium channel; cardiac hypertrophy; cardiomyocyte; caveolin
Affiliations: From the Cellular and Molecular Arrhythmia Research Program, Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706., the Veterans Affairs San Diego Healthcare Systems, San Diego, California 92161, and the Department of Anesthesiology, University of California at San Diego, La Jolla, California 92161., From the Cellular and Molecular Arrhythmia Research Program, Department of Medicine, University of Wisconsin, Madison, Wisconsin 53706, .

Abstract:  Pathological cardiac hypertrophy is characterized by subcellular remodeling of the ventricular myocyte with a reduction in the scaffolding protein caveolin-3 (Cav-3), altered Ca(2+) cycling, increased protein kinase C expression, and hyperactivation of calcineurin/nuclear factor of activated T cell (NFAT) signaling. However, the precise role of Cav-3 in the regulation of local Ca(2+) signaling in pathological cardiac hypertrophy is unclear. We used cardiac-specific Cav-3-overexpressing mice and in vivo and in vitro cardiac hypertrophy models to determine the essential requirement for Cav-3 expression in protection against pharmacologically and pressure overload-induced cardiac hypertrophy. Transverse aortic constriction and angiotensin-II (Ang-II) infusion in wild type (WT) mice resulted in cardiac hypertrophy characterized by significant reduction in fractional shortening, ejection fraction, and a reduced expression of Cav-3. In addition, association of PKCα and angiotensin-II receptor, type 1, with Cav-3 was disrupted in the hypertrophic ventricular myocytes. Whole cell patch clamp analysis demonstrated increased expression of T-type Ca(2+) current (ICa, T) in hypertrophic ventricular myocytes. In contrast, the Cav-3-overexpressing mice demonstrated protection from transverse aortic constriction or Ang-II-induced pathological hypertrophy with inhibition of ICa, T and intact Cav-3-associated macromolecular signaling complexes. siRNA-mediated knockdown of Cav-3 in the neonatal cardiomyocytes resulted in enhanced Ang-II stimulation of ICa, T mediated by PKCα, which caused nuclear translocation of NFAT. Overexpression of Cav-3 in neonatal myocytes prevented a PKCα-mediated increase in ICa, T and nuclear translocation of NFAT. In conclusion, we show that stable Cav-3 expression is essential for protecting the signaling mechanisms in pharmacologically and pressure overload-induced cardiac hypertrophy. 

Retracted: No

PubPeer comments:
 The bands of different groups in red or yellow boxes in Fig 5 appear to look similar. ![file] , 
 Figure 7. Could the authors give an explaination? ![file] ,
Epigenetic effects of inhibition of heat shock protein 90 (HSP90) in human pancreatic and colon cancer
Authors: Ganji Purnachandra Nagaraju
Neha Merchant
Christina Wu
Zhengjia Chen
Gregory B Lesinski
Bassel F El-Rayes
Journal: Cancer letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: Colorectal cancer; DNA methylation; Ganetespib; HSP90; Pancreatic cancer.
Affiliations: Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA., Department of Biostatistics, Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA., Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA. Electronic address: .

Abstract:  Silencing of tumor suppressor and DNA repair genes through methylation plays a role in cancer development, growth and response to therapy in colorectal and pancreatic cancers. Heat shock protein 90 (HSP90) regulates transcription of DNA methyltransferase enzymes (DNMT). In addition, DNMTs are client proteins of HSP90. The aim of this study is to evaluate the effects of HSP90 inhibition on DNA methylation in colorectal and pancreatic cancer cell lines. Our data shows that inhibition of HSP90 using ganetespib resulted in downregulation of mRNA and protein expression of DNMT1, DNMT3A, and DNMT3B in HT-29 and MIA PaCa-2 cell lines. This in turn was associated with a drop in the fraction of methylated cytosine residues and re-expression of silenced genes including MLH-1, P16 and SPARC. These effects were validated in HT-29 tumors implanted subcutaneously in mice following in vivo administration of ganetespib. This work demonstrates the effectiveness of ganetespib, an HSP90 inhibitor in modulating DNA methylation through downregulation of DNMT expression. 

Retracted: No

PubPeer comments:
 Figure 3C. Much more similar than you would expect. https: imgur.com cPF0HJF , 
 #1 ![file] Please find the enclosed full-blot for your reference. I request you kindly remove from the site. Thank you , 
 #1 ![file] Please see full-original blot. I request you please remove or withdraw your comment. thank you ,
RETRACTED ARTICLE: Expression tendency and prognostic value of TCF21 in hepatocellular carcinoma
Authors: Jun-Li Zhang
Peng Du
Jia-Cheng Zhang
Wei Lu
Chao Yang
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: TCF21; hepatocellular carcinoma; prognosis; qRT-PCR.
Affiliations: a Department of Interventional Medicine , Chinese PLA General Hospital-Sixth Medical Center , Beijing , China.

Abstract:  Background: Transcription factor 21 (TCF21) is identified as a tumor suppressor in a variety of human tumors. The purpose of the study was to examine its expression tendency and prognostic value in hepatocellular carcinoma (HCC). Methods: Relative expression of TCF21 mRNA in tissue samples from HCC patients and healthy volunteers were detected through quantitative real-time polymerase chain reaction (qRT-PCR) while its protein level was examined via immunohistochemistry analysis. Chi-square test was adopted to assess the association of TCF21 expression with the clinicopathological characteristic of the patients. Then Kaplan-Meier analysis was employed to analyze the function of TCF21 expression on overall survival among HCC patients. Results: Both the mRNA and protein levels of TCF21 were significantly reduced in HCC tissue samples compared with healthy controls (p &lt; .05). Also, its expression was obviously affected by the classification of tissue pathology, metastasis, T stage, N stage and pathological grading. According to Kaplan-Meier analysis, patients with higher expression of TCF21 experienced dramatically longer overall survival time than those with lower expression (log rank test, p &lt; .001). Conclusions: TCF21 expression was decreased in HCC patients and it could act as a prognostic marker. 

Retracted: Yes

PubPeer comments:
null, 
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 Last author. http: www.nature.com news don-t-run-biomedical-science-as-a-business-1.22366 , 
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 #13 False color image confirms these Figure 2 concerns for me. In addition, see the area identified with the red arrow. This appears to show a small slice of the *left* side of a band. Could the authors please provide the original uncropped scans to address these concerns? *** ![file] ,
Long non-coding RNA SNHG16 regulates cell behaviors through miR-542-3p/HNF4α axis via RAS/RAF/MEK/ERK signaling pathway in pediatric neuroblastoma cells
Authors: Shuangjie Yang
Xiang Wang
Defeng Deng
Journal: Bioscience reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HNF4α; RAS/RAF/MEK/ERK signaling pathway; SNHG16; miR-542-3p; neuroblastoma.
Affiliations: Department of Hematology, Kaifeng Children's Hospital, Kaifeng, Henan, China.

Abstract:  Neuroblastoma (NB) is an extracranial solid tumor in children with complex mechanism. Increasing reports indicated that long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) account for the pathogenesis of NB. Nevertheless, the precise functions of SNHG16 needed to be further exposed in NB progression. Our data revealed that SNHG16 and hepatocyte nuclear factor 4 α (HNF4α) were up-regulated, but miR-542-3p was down-regulated in NB. Knockdown of SNHG16 or HNF4α could impede cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro. Interestingly, the role of SNHG16 detetion in cell behaviors was rescued by HNF4α overexpression in NB cells. Mechanically, SNHG16 modulated the progression of tumor growth via miR-542-3p/HNF4α axis in NB. Also, SNHG16 knockdown inactivated rat sarcoma/effector of RAS/mitogen-activated extracellular signal-regulated kinase/extracellular regulated protein kinases (RAS/RAF/MEK/ERK) signaling pathway through HNF4α. Therefore, SNHG16/miR-542-3p/HNF4α axis modified NB progression via RAS/RAF/MEK/ERK signaling pathway, might highlight a novel therapeutic approach for NB. 

Retracted: No

PubPeer comments:
 Western blots in this paper appear unusual to my eye. Uniform shade seems unexpected and the bands look like they are floating on background. Could the authors comment on the procedure used to generate this figure and provide original scans? Example: ![file] Enhancing the contrast increases my concern: ![file] And after using a thresholding tool the uniformity of the bands become more apparent: ![file] *** The image above is from Figure 2H ![file] ,
miR-663 promotes NPC cell proliferation by directly targeting CDKN2A
Authors: Ning Zhang
Weijun Luo
Zhiqian Lv
Tao Xu
Yanming Deng
Yang Zhang
Shaoen Li
Shaoqiang Liang
Zhenhe Zheng
Lusi Chen
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-663; nasopharyngeal carcinoma; serum levels; lymph node metastasis
Affiliations: Department of Radiotherapy, Tumor Hospital of First People's Hospital of Foshan, Foshan, Guangdong 528041, P.R. China.

Abstract:  MicroRNAs (miRs) act as important regulators during the development and progression of human cancer; however, the regulatory mechanism of miR-663 in nasopharyngeal carcinoma (NPC) remains unclear. The present study demonstrated that serum miR‑663 levels were significantly increased in patients with NPC compared with healthy controls. In addition, the serum levels of miR‑663 were associated with the grade, lymph node metastasis and clinical stage of NPC. The expression of miR‑663 was increased in NPC C666‑1 cells, compared with normal nasopharyngeal epithelial NP69 cells. The knockdown of miR‑663 markedly decreased the proliferation of C666‑1 cells through the induction of cell cycle arrest at the G1 stage. Cyclin‑dependent kinase inhibitor 2A (CDKN2A) was hypothesized to be a putative target of miR‑663. Further investigation confirmed that miR‑663 was able to directly bind to the 3' untranslated region of CDKN2A mRNA, and to negatively regulate CDKN2A protein expression in C666‑1 cells. Inhibition of CDKN2A expression attenuated the suppressive effects of miR‑663 knockdown on the proliferation and cell cycle progression of C666‑1 cells. In addition, it was observed that the mRNA and protein levels of CDKN2A were decreased in C666‑1 cells compared with NP69 cells. In conclusion, the results of the present study demonstrated that miR‑663 promoted the proliferation and cell cycle progression of NPC cells by directly targeting CDKN2A, suggesting that miR‑663 may become a potential therapeutic target for the treatment of NPC. 

Retracted: Yes

PubPeer comments:
 Figs 2D, 5C. ![file] For comparison: Figs 3E, 4E from [Huang et al (2013)] : ![file] Figs 2C, 2F, 4E, 4F from [Su et al (2017)] : ![file] Fig 6A B from [Li et al (2014)] : ![file] Shared panels are marked. , 
 Retracted [22 November 2021] . -------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that certain of the cell cycle assay data shown in Figs. 2D and 5C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Molecular Medicine Reports*, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. ,
MicroRNA-205 functions as a tumor suppressor in colorectal cancer by targeting cAMP responsive element binding protein 1 (CREB1)
Authors: Wan-Jiang Xue
Peng Li
Ying Feng
Qin-Sheng Mao
Journal: American journal of translational research (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Colorectal cancer; cAMP responsive element binding protein 1; miR-205.
Affiliations: Department of Surgery, Affiliated Hospital of Nantong University Nantong 226001, China.

Abstract:  Background: MicroRNAs (miRNA) have been documented playing critical roles in cancer progression. Aberrant expression of miR-205 has been reported in several types of cancer. However, the role and mechanism of miR-205 in colorectal cancer (CRC) remains unclear. Methods: In this study, the expression levels of miR-205 in CRC tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR). MTT assay and transwell assays were applied to assess the effect of miR-205 on CRC cell proliferation, migration and invasion abilities in vitro. Furthermore, Dual-luciferase reporter assay was conducted to confirm the direct binding of miR-205 and target genes. Results: In the present study, we found that the expression level of miR-205 in CRC tissues and cell lines was significantly down-regulated. Functional assays showed that overexpression of miR-205 suppressed CRC cell proliferation, migration and invasion in vitro. In addition, cAMP responsive element binding protein 1 (CREB1) was identified as targets of miR-205. Silencing CREB1 had similar effects of miR-205 restoration on proliferation, migration and invasion in CRC cells. Conclusions: Our results demonstrated that miR-205 may act as a tumor suppressor by targeting the CREB1 gene and suppressing CRC cell proliferation, migration and invasion. Thus, miR-205 may represent a potential therapeutic target for CRC intervention. 

Retracted: No

PubPeer comments:
 Figs 2D, 4C.  miR205 suppressed the invasion ability of of SW480 and HT29 cells ;  Transfection of si-CREB1 suppressed SW480 cell migration and invasion ability . ![file] The treatments seem to be different. ,
Lentinan Inhibits AGE-Induced Inflammation and the Expression of Matrix-Degrading Enzymes in Human Chondrocytes
Authors: Zhuqing Zha
Zhaozhen Zhang
Wuyin Li
Zhiwei Zhao
Wenjing Liu
Journal: Drug Design Development and Therapy (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: AGEs; NF-κB; chondrocytes; lentinan; osteoarthritis.
Affiliations: Department of Bone Surgery, Luoyang Orthopedic Hospital of Henan Province (Henan Provincial Orthopedic Hospital), Zhengzhou City, Henan Province 450000, People's Republic of China.

Abstract:  Background: Chondrocyte-mediated inflammation is an important pathological component of osteoarthritis (OA) development. There are currently no therapies that completely reverse the development of OA. Lentinan, a type of polysaccharide derived from Lentinus edodes, has been demonstrated to possess significant anti-viral, anti-cancer, and anti-inflammatory effects, and has been recently used in the treatment of several inflammatory diseases. However, little research has focused on the pharmacological effect of lentinan in human OA. Materials and methods: We evaluated the anti-inflammatory and anti-ROS effects of lentinan in SW1353 chondrocytes treated with AGEs using real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and the nitro oxide-specific stain DAF-FM DA. The regulatory effects of lentinan on NF-κB and MAPK p38 signaling were investigated via promoter assay and Western blot analysis. Results: We found that lentinan inhibits the production of pro-inflammatory cytokines, including IL-1β, TNF-α, IL-8 and the secretion of PGE2 and NO, by reducing the expression of COX-2 and iNOS in AGE-challenged chondrocytes. Lentinan also reduces AGE-induced increased expression of matrix metalloproteinases-1, -3, and -13 (MMP-1, MMP-3, MMP-13). Furthermore, lentinan has a similar effect on a disintegrin and metalloproteinase with thrombospondin motifs-4 and -5 (ADAMTS-4, ADAMTS-5). Mechanistically, lentinan reduces the activation of NF-κB. Conclusion: Our findings indicate that lentinan shows a protective effect against AGE-induced inflammatory response in chondrocytes. These findings suggest that lentinan is a promising agent for the treatment of OA that could be used as a dietary supplement for patients with OA. 

Retracted: No

PubPeer comments:
 Something odd has happened with the WBs in Figure 6. Could the authors check the blots and perhaps upload uncropped images? The beta-actin controls fall on a pixel-perfect line - I ve added in a straight line offset by three pixels to illustrate the problem. The chances that four consecutive blots would fall on the same line for a marker that s run half-way through a gel are astronomical. ![file] Moreover, there is no mention of stripping or reblotting. Yet beta-actin p-38 nad p-p-38 are all of roughly the same size. How were they blotted on the same membrane? ,
Evaluation of METase-pemetrexed-loaded PEG–PLGA nanoparticles modified with anti-CD133–scFV for treatment of gastric carcinoma
Authors: Lin Xin
Hou-Ting Zhang
Yi-Fan Li
Wei-Feng Yang
Chuan Liu
Journal: Bioscience Reports (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CD133; PEG-PLGA nanoparticles; gastric carcinoma; methioninase; pemetrexed
Affiliations: Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China ., Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.

Abstract:  PEG-PLGA nanoparticles (NPs) modified with anti-CD133 and tumor-targeting single-chain antibody fragment (scFV-NPs) for systemic delivery of methioninase (METase) and pemetrexed for gastric carcinoma were successfully formulated. The structure characterization and biological functions of METase-pemetrexed-loaded scFV-PEG-PLGA NPs (scFV-METase/pemetrexed-NPs) in vitro were investigated. Functional scFV-PEG-PLGA NPs or PEG-PLGA NPs present low cell cytoxicity in CD133+ SGC7901 cells. scFV-METase/pemetrexed-NPs (scFv-M/P-NP) was more effective in inhibiting tumor growth (including cell growth and migration ability) in CD133 positive expressed gastric cancer cells than METase/pemetrexed-NPs (M/P-NP). Moreover, METase enhanced the inhibitory effect of pemetrexed on thymidylate synthase (TS) synthesis and cell apoptosis. We have demonstrated the application of scFV-targeted PEG-PLGA NPs as a new potential strategy to enhance treatment benefits for gastric carcinoma. 

Retracted: No

PubPeer comments:
 December 16, 2020 The authors of the original article u201cEvaluation of METase-Pemetrexed-Loaded PEG-PLGA Nanoparticles Modified with Anti-CD133-scFV for Treatment of Gastric Carcinomau201d (Biosci Rep (2018) 38(1), DOI: 10.1042 BSR20171001) would like to correct Figure 2C. During the authors figure build of Figure 2C, the migration images in the u201cCD133-u201d group and the u201cCD133+u201d group had been switched. The authors declare that these corrections do not change the results or conclusions of their paper, and would like to apologize for any inconvenience caused. All of the authors have approved the correction. The correct version of Figure 2 is presented here. ![file] *** Original image in Figure 2C ![file] The image overlap does not appear to be explained in the correction text. , 
 EXPRESSION OF CONCERN| FEBRUARY 16 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Long noncoding RNA ITGB2‐AS1 promotes growth and metastasis through miR‐4319/RAF1 axis in pancreatic ductal adenocarcinoma
Authors: Heshui Wu
Ming Yang
Junling Zhu
Chunyou Wang
Yao Guo
Qi Qin
Tao Yin
Journal: Journal of Cellular Physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ITGB2-AS1; PDAC; RAF1; miR-4319; progression.
Affiliations: Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China., Department of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China., Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Abstract:  Long noncoding RNA (lncRNA) has been considered as potentially critical regulators in pancreatic ductal adenocarcinoma (PDAC). In this study, we prospectively investigate the effect and mechanism of lncRNA integrin subunit beta 2-anti-sense RNA 1 (ITGB2-AS1) on regulation of PDAC progression. The expression of ITGB2-AS1 and its target were analyzed by quantitative real-time polymerase chain reaction and in situ hybridization. 3-(4,5-Dimethylthiazol-z-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, wound healing, and transwell assays were used to investigate the influence of ITGB2-AS1 on cell proliferation, cell cycle, migration, and invasion, respectively. The interaction between ITGB2-AS1 and its target was determined via luciferase activity assay and RNA immunoprecipitation. The subcutaneous xenotransplanted tumor model was established and employed to detect the tumorigenic function of ITGB2-AS1, which was evaluated by western blot analysis, immunohistochemistry, and hematoxylin and eosin staining. The results showed that ITGB2-AS1 was elevated in both PDAC tumor tissues and cell lines, predicting a poor prognosis in PDAC patients. Knocking down of ITGB2-AS1 suppressed PDAC cell proliferation, invasion, and migration but induced cell apoptosis in vitro. Moreover, ITGB2-AS1 could target and inhibit the expression of miR-4319 and miR-4319-targeted and -suppressed serine/threonine kinase RAF1. ITGB2-AS1 promoted PDAC progression via inhibition of miR-4319. Interference of ITGB2-AS1 could suppress in vivo tumorigenic ability of PDAC via downregulation of RAF1. In conclusion, ITGB2-AS1 promoted PDAC progression via sponging miR-4319 to upregulate RAF1, suggesting the potential therapeutic target ability of ITGB2-AS1 in PDAC. 

Retracted: No

PubPeer comments:
 In Figure 3a and 6c, micrographs have been duplicated and presented as something else. ![file] , 
 We also found the problem, because there were too many experimental images, we mixed up some images when organizing and writing articles. We have sent the correct figures to the journal and asked them to help us replace the wrong ones. Because my paper is still in an early view, they can make the corrections. Once the production editor informs me that the final version has been released, I will upload the link of the final and correct version in time. ---Ming Yang ,
The conformational state of polyphenol oxidase from field bean (Dolichos lablab) upon SDS and acid-pH activation
Authors: A G Appu Rao
Santosh R Kanade
Beena Paul
Lalitha R Gowda
Journal: Biochemical Journal (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Field bean; PPO; polyphenol oxidase; activation; pH optimum
Affiliations: Department of Protein Chemistry and Technology, Central Food Technological Research Institute (CFTRI), Mysore-570 020, India

Abstract:  Field bean (Dolichos lablab) contains a single isoform of PPO (polyphenol oxidase)--a type III copper protein that catalyses the o-hydroxylation of monophenols and oxidation of o-diphenols using molecular oxygen--and is a homotetramer with a molecular mass of 120 kDa. The enzyme is activated manyfold either in the presence of the anionic detergent SDS below its critical micellar concentration or on exposure to acid-pH. The enhancement of kcat upon activation is accompanied by a marked shift in the pH optimum for the oxidation of t-butyl catechol from 4.5 to 6.0, an increased sensitivity to tropolone, altered susceptibility to proteolytic degradation and decreased thermostability. The Stokes radius of the native enzyme is found to increase from 49.1+/-2 to 75.9+/-0.6 A (1 A=0.1 nm). The activation by SDS and acid-pH results in a localized conformational change that is anchored around the catalytic site of PPO that alters the microenvironment of an essential glutamic residue. Chemical modification of field bean and sweet potato PPO with 1-ethyl-3-(3-dimethylaminopropyl)carbodi-imide followed by kinetic analysis leads to the conclusion that both the enzymes possess a core carboxylate essential to activity. This enhanced catalytic efficiency of PPO, considered as an inducible defence oxidative enzyme, is vital to the physiological defence strategy adapted by plants to insect herbivory and pathogen attack. 

Retracted: No

PubPeer comments:
 ![file] , 
 #1 That s pretty weak. I would not be willing to place a wager in support of your claim. Here s another view of the same region, after adjusting the gradient map: ![file] , 
 #2 Lane 11 is the lane under question. There are quite a lot of similarities between the upper and lower lanes. , 
 ![file] ,
Retracted: Immunoglobulin G4 + B‐cell receptor clones distinguish immunoglobulin G 4‐related disease from primary sclerosing cholangitis and biliary/pancreatic malignancies
Authors: Emma L Culver
Paul L Klarenbeek
Frank Baas
Stan F van de Graaf
Roger W Chapman
Eleanor Barnes
Joanne Verheij
Lowiek M Hubers
Niek de Vries
Marieke E Doorenspleet
Ulrich Beuers
Lucas J Maillette de Buy Wenniger
Thomas M van Gulik
Journal: Hepatology (2016)
Discipline: CLINICAL MEDICINE
Keywords: Immunoglobulin G4; IgG4-related disease; B-cell receptor; next-generation sequencing; primary sclerosing cholangitis
Affiliations: Amsterdam Rheumatology and Immunology Center, Department of Clinical Immunology & Rheumatology, Academic Medical Center, Amsterdam, The Netherlands., Department of Gastroenterology & Hepatology and Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, Amsterdam, The Netherlands., Translational Gastroenterology Unit, John Radcliffe Hospital, Oxford, United Kingdom., Department of Genome Analysis, Academic Medical Center, Amsterdam, The Netherlands., Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands., Department of Surgery, Academic Medical Center, Amsterdam, The Netherlands.

Abstract:  Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) of the biliary tree and pancreas is difficult to distinguish from sclerosing cholangitis and biliary/pancreatic malignancies (CA). An accurate noninvasive test for diagnosis and monitoring of disease activity is lacking. We demonstrate that dominant IgG4(+) B-cell receptor (BCR) clones determined by next-generation sequencing accurately distinguish patients with IgG4-associated cholangitis/autoimmune pancreatitis (n = 34) from those with primary sclerosing cholangitis (n = 17) and CA (n = 17). A novel, more affordable, and widely applicable quantitative polymerase chain reaction (qPCR) protocol analyzing the IgG4/IgG RNA ratio in blood also achieves excellent diagnostic accuracy (n = 125). Moreover, this qPCR test performed better than serum IgG4 levels in sensitivity (94% vs. 86%) and specificity (99% vs. 73%) and correlates with treatment response (n = 20). Conclusions: IgG4(+) BCR clones and IgG4/IgG RNA ratio markedly improve delineation, early diagnosis, and monitoring of IgG4-RD of the biliary tree and pancreas. (Hepatology 2016;64:501-507). 

Retracted: Yes

PubPeer comments:
 2022 retraction. https: aasldpubs.onlinelibrary.wiley.com doi 10.1002 hep.32246 The above article, published online on 25 March 2016 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor in Chief Dr. David Cohen, and Wiley Periodicals LLC. The retraction was requested by the authors because upon re-analysis, they concluded that the qPCR results reported in the article were incorrect. ,
Supercoiling and denaturation in Gal repressor/heat unstable nucleoid protein (HU)-mediated DNA looping
Authors: David Dunlap
Sankar Adhya
Jean-Francois Allemand
Giuseppe Lia
Dale E A Lewis
Laura Finzi
Vincent Croquette
David Bensimon
Journal: Proceedings of the National Academy of Sciences of the United States of America (2003)
Discipline: Multidisciplinary
Keywords: DNA topology; transcription regulation; Gal repressor; DNA looping; supercoiling
Affiliations: Department of Biology, University of Milan, 20133 Milan, Italy.

Abstract:  The overall topology of DNA profoundly influences the regulation of transcription and is determined by DNA flexibility as well as the binding of proteins that induce DNA torsion, distortion, and/or looping. Gal repressor (GalR) is thought to repress transcription from the two promoters of the gal operon of Escherichia coli by forming a DNA loop of approximately 40 nm of DNA that encompasses the promoters. Associated evidence of a topological regulatory mechanism of the transcription repression is the requirement for a supercoiled DNA template and the histone-like heat unstable nucleoid protein (HU). By using single-molecule manipulations to generate and finely tune tension in DNA molecules, we directly detected GalR/HU-mediated DNA looping and characterized its kinetics, thermodynamics, and supercoiling dependence. The factors required for gal DNA looping in single-molecule experiments (HU, GalR and DNA supercoiling) correspond exactly to those necessary for gal repression observed both in vitro and in vivo. Our single-molecule experiments revealed that negatively supercoiled DNA, under slight tension, denatured to facilitate GalR/HU-mediated DNA loop formation. Such topological intermediates may operate similarly in other multiprotein complexes of transcription, replication, and recombination. 

Retracted: No

PubPeer comments:
 In 2014, the authors used the data of gene polymorphism as a master s thesis, and in 2017, she published a article in Chin J Oncol (DOI: 10.3760 cma.j. issn.0253-3766.2017.02.009) using the same data. Amazing, in 2020, the same authors published similar article in Journal of cellular biochemistry (DOI: 10.1002 jcb.29135) with the same data and pictures. In general, the same authors published articles in Chinese and English using the same data and pictures. Figure 3 (B) in article published in Chin J Oncol, ![file] Figure 1 (D) in article published in Journal of cellular biochemistry, ![file] Similarly, Figure 3 (A) in article published in Chin J Oncol, ![file] Figure 1 (D) in article published in Journal of cellular biochemistry, ![file] ,
Curcumin downregulates cell survival mechanisms in human prostate cancer cell lines
Authors: B B Aggarwal
A Mukhopadhyay
P Pantazis
C Bueso-Ramos
D Chatterjee
Journal: Oncogene (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NF-kappaB; AP-1; prostate cancer cells; proliferation; survival
Affiliations: Cytokine Research Laboratory, Department of Bioimmunotherapy, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

Abstract:  While the role of nuclear transcription factor activator protein-1 (AP-1) in cell proliferation, and of nuclear factor-kappaB (NF-kappaB) in the suppression of apoptosis are known, their role in survival of prostate cancer cells is not well understood. We investigated the role of NF-kappaB and AP-1 in the survival of human androgen-independent (DU145) and -dependent (LNCaP) prostate cancer cell lines. Our results show that the faster rate of proliferation of DU145 cells when compared to LNCaP cells correlated with the constitutive expression of activated NF-kappaB and AP-1 in DU-145 cells. The lack of constitutive expression of NF-kappaB and AP-1 in LNCaP cells also correlated with their sensitivity to the antiproliferative effects of tumor necrosis factor (TNF). TNF induced NF-kappaB activation but not AP-1 activation in LNCaP cells. In DU145 cells both c-Fos and c-Jun were expressed and treatment with TNF activated c-Jun NH2-terminal kinase (JNK), needed for AP-1 activation. In LNCaP cells, however, only low levels of c-Jun was expressed and treatment with TNF minimally activated JNK. Treatment of cells with curcumin, a chemopreventive agent, suppressed both constitutive (DU145) and inducible (LNCaP) NF-kappaB activation, and potentiated TNF-induced apoptosis. Curcumin alone induced apoptosis in both cell types, which correlated with the downregulation of the expression of Bcl-2 and Bcl-xL and the activation of procaspase-3 and procaspase-8. Overall, our results suggest that NF-kappaB and AP-1 may play a role in the survival of prostate cancer cells, and curcumin abrogates their survival mechanisms. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] ,