PReD-Bench/PRed-Bench huggingface dataset:
Egr-1 Induces the Expression of Its Corepressor Nab2 by Activation of the Nab2 Promoter Thereby Establishing a Negative Feedback Loop
Authors: Joerg Kumbrink
Judith P Johnson
Marco Gerlinger
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: transcription factor; Egr-1; corepressors; Nab1; Nab2

Abstract:  The transcription factor Egr-1 regulates the expression of numerous genes involved in differentiation, growth, and in response to environmental signals. Egr-1 activity is modulated in part through the binding of corepressors Nab1 and Nab2. Nab2 appears crucial for controlling Egr-1-mediated transactivation because it is a delayed early response gene, induced by the same stimuli that induce the immediate early gene Egr-1. To identify important elements regulating Nab2 expression, we cloned the human Nab2 gene and investigated the 5'-region. The TATA- and initiator-less Nab2 promoter, located from -679 to -74 bp, contains a total of 11 Egr binding sites, including a cluster of multiple overlapping Egr/Sp1 sites between -329 and -260 bp. This region is critical for basal promoter activity as well as for maximum induction by phorbol esters. Electromobility shifts show that Sp1 binds to this region in normal and stimulated cells, whereas stimulation induces binding of Egr-1. In addition Egr-1 activates the Nab2 promoter in a pattern similar to phorbol esters, suggesting that Egr-1 is a major inducer of protein kinase C-mediated Nab2 induction. Depletion of Egr-1 by each of two distinct Egr-1 short-interfering RNAs reduces Nab2 expression and inducibility, confirming that Egr-1 is an important regulator of Nab2 expression. Transfection experiments show that Egr-1-induced Nab2 promoter activity is itself repressed by Nab2. These results indicate that Egr-1 mediates the induction of its own repressor, thereby preventing a permanent transactivation of Egr-1 target genes and a damaging overreaction in response to environmental signals. 

Retracted: No

PubPeer comments:
 Fig.3A There are visible splice line. Could the authors explain this? ![file] ,
Long noncoding RNA FAM3D-AS1 inhibits development of colorectal cancer through NF-κB signaling pathway
Authors: Feng Yu
Ying Meng
Journal: Bioscience Reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Colorectal cancer; EMT; lncRNA.
Affiliations: The First Division of Cancer Department of Zibo Central Hospital, Shandong, China., The Second Division of Gastroenterology Department of Zibo Central Hospital, Shandong, China .

Abstract:  Although numerous differential long noncoding RNAs (IncRNAs) have been identified, the relationship between lncRNA and colorectal cancer (CRC) still remains largely unclear. In the present study, we investigated the function and provided a possible mechanism of lncRNA FAM3D-AS1 in CRC. CCK8, transwell, and trypan blue staining were used to evaluate the proliferation, invasion, and cell death rates. Real-time PCR was used to elucidate the expression level of FAM3D-AS1. We found that lncRNA FAM3D-AS1 located in cytoplasm. Overexpression of FAM3D-AS1 significantly inhibited the cell proliferation, cell survival rates, and invaded cells. We also provided evidence that FAM3D-AS1 reversed the EMT process. Moreover, we proved that FAM3D-AS1 inhibits CRC development through NF-κB signaling pathway. Taken together, we performed functional analysis of FAM3D-AS1 and provided a possible mechanism in the development of CRC. Our study provided new targets for clinical treatment. 

Retracted: No

PubPeer comments:
 Figure 3(C) seems confused. *** ![file] , 
 April 7, 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. ,
Noxa mediates bortezomib induced apoptosis in both sensitive and intrinsically resistant mantle cell lymphoma cells and this effect is independent of constitutive activity of the AKT and NF-kappaB pathways
Authors: Raymond Lai
Helena Mora-Jensen
Federica Gibellini
Edgar Gil Rizzatti
Elinor Lee
Masanori Daibata
Marc Andrée Weniger
Adrian Wiestner
Journal: Leukemia & Lymphoma (2008)
Discipline: CLINICAL MEDICINE
Keywords: Bortezomib; mantle cell lymphoma; resistance; proteasome; Noxa
Affiliations: Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.

Abstract:  Bortezomib is more active against mantle cell lymphoma (MCL) than against most other lymphoma subtypes. Nevertheless, up to half of patients with MCL have bortezomib resistant disease. Factors contributing to intrinsic resistance to bortezomib have not been determined. Here we used a panel of eight bortezomib sensitive (median IC(50) 5.9 nM) and three relatively bortezomib resistant cell lines (median IC(50) 12.9 nM) to investigate differences in tumor biology that could determine sensitivity to bortezomib. Bortezomib effectively inhibited high baseline proteasome activity and induced a comparable degree of proteasome inhibition in both sensitive and resistant cells. At 10 nM, bortezomib induced the proapoptotic BH3-only protein Noxa in sensitive but not resistant cells. At higher concentrations of bortezomib, however, Noxa was also upregulated in resistant cells and this effect was sufficient to induce apoptosis. Silencing of Noxa with siRNA rescued these cells from apoptosis, arguing against a defect in Noxa regulation or function as the basis of bortezomib resistance. Bortezomib was equally effective against cells with high and low constitutive NF-kappaB signaling. Also, sensitive and resistant MCL cell lines showed comparable activation of the AKT pathway. We conclude that bortezomib can overcome classic mechanisms of resistance to apoptosis and that determinants of bortezomib sensitivity in MCL are due to differences in signaling or stress pathways upstream of Noxa. 

Retracted: No

PubPeer comments:
 In their paper, Tian et al state  Herein, a double log equation was applied to determine both the binding constant and the number of binding sites as follows (van de Weert and Stella 2011). Subsequently showing the following equation: log((F0u2212F) F)=logK+nlog[Q] As the first author of the article cited in support of this equation, I am extremely saddened to see yet another group that has apparently failed to understand the content of Van de Weert and Stella, 2011 . In our article, we actually showed that this double log equation has numerous pitfalls, all of which Tian et al seemed to have ignored. Moreover, we explicitly point out that the equation can only return the number of binding sites under special conditions - and that it in reality just returns the Hill coefficient. Notably, Tian et al are not the first to inappropriately cite Van de Weert and Stella, 2011, in support of this equation. In fact, we even wrote an article on this misrepresentation: https: doi.org 10.1016 j.molstruc.2019.03.024 ,
Diagnostic value of joint detection of homocysteine and RDW CV on acute myocardial infarction
Authors: L-J Qiao
Y-H Li
G-X Hu
L Mou
Y-G Tian
J Zhang
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Diagnostic value; joint detection; homocysteine; RDW CV; acute myocardial infarction
Affiliations: Department of Intensive Medicine, Shengli Oilfield Central Hospital, Dongying, Shandong, China.

Abstract:  The article "Diagnostic value of joint detection of homocysteine and RDW CV on acute myocardial infarction" by G.-X. Hu, J. Zhang, Y.-G. Tian, Y.-H. Li, L. Mou, L.-J. Qiao, published in Eur Rev Med Pharmacol Sci 2016; 20 (19): 4124-4128 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
lincRNAs act in the circuitry controlling pluripotency and differentiation
Authors: Xiaoping Yang
Robert Ach
Mitchell Guttman
Geneva Young
John L Rinn
Laurakay Bruhn
Julie Donaghey
Ido Amit
Glen Munson
Eric S Lander
Aviv Regev
Bryce W Carey
Alexander Meissner
Manuel Garber
David E Root
Anne Bergstrom Lucas
Jennifer K Grenier
Journal: Nature (2011)
Discipline: Multidisciplinary
Keywords: lincRNAs; gene expression; mouse embryonic stem cells; pluripotent state; lineage commitment programs
Affiliations: Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. 

Abstract:  Although thousands of large intergenic non-coding RNAs (lincRNAs) have been identified in mammals, few have been functionally characterized, leading to debate about their biological role. To address this, we performed loss-of-function studies on most lincRNAs expressed in mouse embryonic stem (ES) cells and characterized the effects on gene expression. Here we show that knockdown of lincRNAs has major consequences on gene expression patterns, comparable to knockdown of well-known ES cell regulators. Notably, lincRNAs primarily affect gene expression in trans. Knockdown of dozens of lincRNAs causes either exit from the pluripotent state or upregulation of lineage commitment programs. We integrate lincRNAs into the molecular circuitry of ES cells and show that lincRNA genes are regulated by key transcription factors and that lincRNA transcripts bind to multiple chromatin regulatory proteins to affect shared gene expression programs. Together, the results demonstrate that lincRNAs have key roles in the circuitry controlling ES cell state. 

Retracted: No

PubPeer comments:
 Supplemental Fig. S6 u2013 possible duplication between panels ![file] , 
 The authors claim that dozens of lincRNA control pluripotency and differentiation of stem cells. These authors were only able to knock down some lincRNA by 10-30% and I don t see how such low knock down can be significant. I m struck by such dramatic claims for extremely low knock down efficiency. They also claim lincRNA have trans function but later in 2015 the same Lander group disproved itself. ,
Testosterone Induces Cytoprotection by Activating ATP-Sensitive K + Channels in the Cardiac Mitochondrial Inner Membrane
Authors: Natig Gassanov
Francisco Rivero
Fikret Er
Uta C Hoppe
Guido Michels
Journal: Circulation (2004)
Discipline: CLINICAL MEDICINE
Keywords: Testosterone; Myocardial function; Ischemia/reperfusion injury; Mitochondrial K(ATP) channels; Sarcoplasmatic K(ATP) channels
Affiliations: Department of Internal Medicine III, University of Cologne, Cologne, Germany., From the Department of Internal Medicine III (F.E., G.M., N.G., U.C.H.), Center of Biochemistry I (F.R.), and Center for Molecular Medicine (G.M., F.R., U.C.H.), University of Cologne, Cologne, Germany.

Abstract:  Background: Whereas in the past, androgens were mainly believed to exert adverse effects on the cardiovascular system, recent experimental data postulate a benefit of testosterone for recovery of myocardial function after ischemia/reperfusion injury. Thus, we examined whether testosterone might improve myocardial tolerance to ischemia due to activation of mitochondrial (mitoK(ATP)) and/or sarcoplasmatic (sarcK(ATP)) K(ATP) channels. Methods and results: In a cellular model of ischemia, testosterone significantly decreased the rate of ischemia-induced death of cardiomyocytes that could be prevented by 5-hydroxydecainoic acid but was unaffected by the sarcK(ATP) blocker HMR1098 and the testosterone receptor antagonist flutamide. To index mitoK(ATP), mitochondrial flavoprotein fluorescence was measured. Testosterone induced a highly significant increase in mitochondrial flavoprotein fluorescence in intact myocytes and isolated mitoplasts that could be abolished by 5-hydroxydecainoic acid. Testosterone-mediated flavoprotein oxidation of mitoplasts was K+ dependent and ATP sensitive. In mitoplast-attached single-channel recordings, testosterone directly activated an ATP-sensitive K+ channel of the inner mitochondrial membrane. Addition of the K(ATP) channel opener diazoxide and pinacidil to the cytosolic solution activated the ATP-sensitive K+ current comparable to testosterone, whereas 5-hydroxydecainoic acid and glibenclamide inhibited the testosterone-induced current. Patch-clamp experiments of intact myocytes in whole-cell configuration did not demonstrate any effect of testosterone on sarcK(ATP) channels. Conclusions: Our results provide direct evidence for the existence of cardiac mitoK(ATP) and a link between testosterone-induced cytoprotection and activation of mitoK(ATP). Endogenous testosterone might play a more important role in recovery after myocardial infarction than is currently assumed. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] ,
Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury
Authors: Lianfeng Wu
Weilong Hong
Yong Liang
Hong Lu
Bicheng Chen
Yongheng Bai
Yongyu Bai
Journal: Mediators of Inflammation (2016)
Discipline: IMMUNOLOGY
Keywords: Macrophage migration inhibitory factor (MIF); inflammation; collagen deposition; renal injury; matrix accumulation
Affiliations: Department of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China., Key Laboratory of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.

Abstract:  Background. Macrophage migration inhibitory factor (MIF) is an important immunoregulatory cytokine involved in inflammation, which may be one important reason resulting in matrix deposition in renal tissues after injury. However, the underlying mechanisms have not yet been elucidated. Methods and Results. We uncovered a crucial role of MIF in inflammation and collagen deposition in vivo and in vitro. In rats, ureteral obstruction induced tubular injury, matrix accumulation, and inflammatory cell infiltration. Additionally, enhanced MIF levels in the obstructed kidneys were closely related to the increasing numbers of CD68-positive macrophages. These obstruction-induced injuries can be relieved by recanalization, consequently resulting in downregulated expression of MIF and its receptor CD74. Similarly, ischemia reperfusion induced renal injury, and it was accompanied by elevated MIF levels and macrophages infiltration. In cultured tubular epithelial cells (TECs), aristolochic acid (AA) promoted matrix production and increased MIF expression, as well as the release of macrophage-related factors. Inhibition of MIF with an antagonist ISO-1 resulted in the abolishment of these genotypes in AA-treated TECs. Conclusion. MIF plays an important role in macrophage-related inflammation and matrix deposition in kidney tissues following injury. MIF as a specific inhibitor may have therapeutic potential for patients with inflammatory and fibrotic kidney diseases. 

Retracted: No

PubPeer comments:
 A picture in this paper has been published twice in Chinese papers. ![file] ![file] ![file] ![file] ![file] ![file] ![file] , 
 ![file] , 
 Dear Dr. Tetralia glaberrima Thank you for pointing out the oversights, we have submitted a correction applied to the journal as soon as possible. Thanks again for your work. If there is any need, please contact us at any time. Yours sincerely, Yongheng Bai ,
Down Regulation of ackA-pta Pathway in Escherichia coli BL21 (DE3): A Step Toward Optimized Recombinant Protein Expression System
Authors: Nahid Bakhtiari
Valiollah Babaeipour
Manouchehr Mirshahi
Abbas Tahzibi
Nader Maghsoudi
Journal: Jundishapur Journal of Microbiology (2014)
Discipline: MICROBIOLOGY
Keywords: Acetate; Antisense RNA; Down-Regulation; Escherichia coli.

Abstract:  Background: One of the most important problems in production of recombinant protein is to attain over-expression of the target gene and high cell density. In such conditions, the secondary metabolites of bacteria become toxic for the medium and cause cells to die. One of these aforementioned metabolites is acetate, which enormously accumulated in the medium, so that both cell and protein yields are affected. Objectives: To overcome this problem, several strategies applied. In this research we used antisense RNA strategy, where the transcription of phosphotransacetylase (PTA) and acetate kinase (ACK), two acetate pathway key enzymes, could be controlled, which led to reduced acetate production. Materials and methods: In order to achieve this, recombinant plasmid harboring antisense sequences targeting both of pta and ackA was assembled, after transfecting to the cells, its effects on the cell growth and acetate accumulation in the minimal media was assessed and compared with the control, the plasmid without antisense cassette, in presence and absence of IPTG in Escherichia coli BL21 (DE3). Results: It was observed that the mentioned strategy partially affect the growth and amount of excreted acetate in comparison with the control. In addition it was found that high down-regulation of the acetate production pathway reduces the growth rate of E. coli BL21 (DE3). Conclusions: The study principally proved the importance of this strategy in acetate excretion control. 

Retracted: No

PubPeer comments:
 Figure 2. Some unexpected similarities between the band shown in lane 1 (pLT10T3) and lane 3 (pL6). Highlighted with yellow boxes. ![file] Here is a close up of the relevant area. Intensities of the bands are different and compression artefacts make this hard to visualize. But there is a distinct  m or sideways  3 visible in the bands themselves. In addition, the position of several light spots in the background above both bands appears to match. ![file] ,
Wide-Bandgap Perovskite Quantum Dots in Perovskite Matrix for Sky-Blue Light-Emitting Diodes
Authors: So Min Park
Oleksandr Voznyy
Yitong Dong
Sam Teale
Edward H Sargent
Jian Xu
Jianan Erick Huang
Dongxin Ma
Yuan Liu
Ziliang Li
Bin Chen
Seungjin Lee
Journal: Journal of the American Chemical Society (2022)
Discipline: CHEMISTRY
Keywords: perovskite matrix; quantum dots; red light-emitting diodes; wide-band gap; CsPbBr3
Affiliations: Department of Electrical and Computer Engineering, University of Toronto, 35 St George Street, Toronto M5S 1A4, Ontario, Canada, Department of Physical and Environmental Sciences, University of Toronto, Scarborough, 1065 Military Trail, Toronto M1C 1A4, Ontario, Canada

Abstract:  The epitaxial growth of a perovskite matrix on quantum dots (QDs) has enabled the emergence of efficient red light-emitting diodes (LEDs) because it unites efficient charge transport with strong surface passivation. However, the synthesis of wide-band gap (Eg) QD-in-matrix heterostructures has so far remained elusive in the case of sky-blue LEDs. Here, we developed CsPbBr3 QD-in-perovskite matrix solids that enable high luminescent efficiency and spectral stability with an optical Eg of over 2.6 eV. We screened alloy candidates that modulate the perovskite Eg and allow heteroepitaxy, seeking to implement lattice-matched type-I band alignment. Specifically, we introduced a CsPb1-xSrxBr3 matrix, in which alloying with Sr2+ increased the Eg of the perovskite and minimized lattice mismatch. We then developed an approach to passivation that would overcome the hygroscopic nature of Sr2+. We found that bis(4-fluorophenyl)phenylphosphine oxide strongly coordinates with Sr2+ and provides steric hindrance to block H2O, a finding obtained by combining molecular dynamics simulations with experimental results. The resulting QD-in-matrix solids exhibit enhanced air- and photo-stability with efficient charge transport from the matrix to the QDs. LEDs made from this material exhibit an external quantum efficiency of 13.8% and a brightness exceeding 6000 cd m-2. 

Retracted: No

PubPeer comments:
 In Supplementary Figure 14C, duplicated curves with unexpected noise pattern was observed the sample under 10 V and 12 V. Can the author check the raw data and clarify here? ![file] ,
In vivo anti-apoptosis activity of novel berberine-loaded chitosan nanoparticles effectively ameliorates osteoarthritis
Authors: Hao Peng
Qi Zhao
Yan Zhou
Bin He
Shi-Qing Liu
Ling Yu
Journal: International Immunopharmacology (2015)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Berberine; Chitosan; Drug release; Nanoparticles; Osteoarthritis.
Affiliations: Department of Orthopedics, Central Laboratory, Renmin Hospital, Wuhan University, Wuhan 430060, China., Department of Orthopedics, Central Laboratory, Renmin Hospital, Wuhan University, Wuhan 430060, China. Electronic address: .

Abstract:  Berberine chloride (BBR) is an isoquinoline alkaloid that possesses promising protective efficacies against osteoarthritis (OA). Nevertheless, the therapeutic agent of this substance in OA is limited by its poor aqueous solubility, low bioavailability and short biological half-life. In this study, chitosan (CS)-based nanoparticles were prepared for the sustained release of BBR. Novel BBR-loaded chitosan nanoparticles (CNs) were successfully synthesized by the ionic cross-linking method. BBR-loaded CNs were spherical and homogeneous in shape. Moreover, they exhibited good stability and had ideal releasing profile in vitro. After intra-articular injection of BBR-loaded CNs, the level of BBR in rat plasma decreased and the retention time in synovial fluid increased compared with free BBR solution. In vivo evaluation of BBR-loaded CNs further showed higher anti-apoptosis activity in the treatment of OA compared with BBR solution at equivalent concentration. This result was evidenced by the changes of gross morphology and histological analyses in rat articular cartilage, TUNEL assay, quantitative real-time polymerase chain reaction, Western blot, and immunohistochemical analyses of caspase-3, Bcl-2 and Bax expressions. Given these results, BBR-loaded CNs are potential therapeutic agents for OA. 

Retracted: No

PubPeer comments:
 Figure 3C. Much more similar than expected. ![file] ,
MiR-363-3p modulates cell growth and invasion in glioma by directly targeting pyruvate dehydrogenase B
Authors: Q-S Zhang
D-X Xu
J-J Guo
G-Y Zhu
T Cui
H-J Wu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-363-3p; cancer development; glioma; PDHB; onco-miRNA
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Henan University of Science and Technology, Henan, China. .

Abstract:  Objective: This study is designed to investigate the role of miR-363-3p in the cancer development of glioma. Patients and methods: The expression of miR-363-3p in glioma and adjacent noncancerous tissue was measured using quantitative RT-PCR. The expression of a target gene of miR-363-3p, pyruvate dehydrogenase B (PDHB), was determined by Western blot. The level of miR-363-3p was increased or decreased by transfected with miR-363-3p mimic or miR-363-3p inhibitor, respectively. The impact of miR-363-3p on cell growth, apoptosis and invasion was determined by CCK-8 (Cell Counting Kit) assay, flow cytometry, and transwell assay. The role of PDHB in mediating the oncogenic activities was demonstrated by co-transfected PDHB vector and miR-363-3p mimic. Results: Our results have shown that miR-3663-3p level was significantly higher in glioma tissue. Furthermore, miR-363-3p functions as onco-miRNA, promotes cell proliferation, protects against apoptosis, and enhances invasion by directly targeting PDHB. Conclusions: MiR-363-3p is an onco-miRNA, which can be considered as a potential therapeutic target in glioma. 

Retracted: No

PubPeer comments:
 Figure 2, 3, and 5 appear to have overlapping images. The controls and the mir-363-3p mimics are covered, but the images in dark blue and fuchsia are labeled differently. ![file] ![file] ![file] ,
microRNA‑372 inhibits proliferation and induces apoptosis in human breast cancer cells by directly targeting E2F1
Authors: Wei-Jian Sun
Jie-Fan Liu
Ya-Xin Zhao
Yao-Jun Yu
Hua-Cheng Liu
Wei-Yang Ying
Cheng-Yu Wang
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Breast cancer; miR-372; cell proliferation; apoptosis; E2F1
Affiliations: Department of General Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China., Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China., Department of General Practice, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, P.R. China.

Abstract:  Breast cancer is the most prevalent cancer and the leading cause of cancer‑associated mortalities among women worldwide today. Accumulating evidence suggested that miR‑372 may serve important roles in the initiation and development of various human cancers. However, the role of miR‑372 in breast cancer remains unknown. The present study demonstrated that the expression level of miR‑372 in human breast cancer tissues and cell lines is significantly reduced compared with normal breast tissues cell lines. Furthermore, results of functional assays indicated that miR‑372 inhibits cell proliferation and induces apoptosis in the MCF‑7 human breast cancer cell line. E2F1 was identified as a direct functional target of miR‑372 in breast cancer. In conclusion, the findings revealed that miR‑372 may have the potential to act as a novel molecule for the diagnosis and therapy of patients with breast cancer. 

Retracted: No

PubPeer comments:
 Fig 2:  Apoptosis rate of transfected MCF-7 cells transfected with miR-372 (E) inhibitors and (F) mimics, as analyzed by flow cytometry ; FIg 4D,  Apoptosis of transfected MCF-7 cells, as analyzed by flow cytometry . Two panels are the same, despite different labels (blue boxes). ![file] Orange boxes mark two panels that have a remarkable number of points in common. Here dramatised by color-reversing one panel and superimposing it on the other, so that shared points cancel out. ![file] There are also many points shared between the blue-marked and orange-marked panels, but I leave that as an exercise. ,
MiR-218 promotes apoptosis of U2OS osteosarcoma cells through targeting BIRC5
Authors: S-F Jing
J-F Gao
X-Y Huang
D-Z Wang
Q-T Miao
S-B Hao
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: BIRC5; miR-218; apoptosis; osteosarcoma; caspase activity
Affiliations: Department of Orthopedics, Zhang Qiu People's Hospital, Zhangqiu, Shandong, China. .

Abstract:  Objective: Baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) is a member of apoptosis inhibition family which suppresses caspase activity. Osteosarcoma tissues have significantly higher BIRC5 and lower microRNA-218 (miR-218) level than adjacent tissues, indicating tumor suppressor role of miR-218 in osteosarcoma. Bioinformatics analysis showed satisfactory targeting correlation between miR-218 and 3'-UTR of BIRC5 mRNA. This study, thus, investigated if dysregulation of miR-218 and BIRC5 affected apoptosis of osteosarcoma cells U2OS. Patients and methods: A total of 42 osteosarcoma patients were collected for tumor and adjacent tissues to compare miR-218 and BIRC5 expressions. Dual-luciferase reporter gene assay examined targeted regulation between miR-218 and BIRC5. In vitro cultured U2OS cells were treated with miR-218 mimic and/or si-BIRC5. Caspase-3 activity was measured by spectrometry while flow cytometry was used to test cell apoptosis, plus protein expression assay by Western blot assay. Results: Compared to adjacent tissues, osteosarcoma tissues had significantly depressed miR-218 expression and elevated BIRC5 expression (p&lt;0.05). miR-21 targeted 3'-UTR of BIRC5 to suppress its expression. The elevation of miR-218 and/or silencing BIRC5 significantly depressed BRIC5-induced inhibition on caspase-5, and facilitated U2OS cell apoptosis (p&lt;0.05). Conclusions: We observed that miR-218 was significantly down-regulated in osteosarcoma tissues, which had elevated BIRC5 expression. MiR-218 targeted and inhibited BIRC5 expression, weakened caspase-5 inhibition by BIRC5, and facilitated U2OS osteosarcoma cell apoptosis. 

Retracted: Yes

PubPeer comments:
 [Retracted] . Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, u201cMiR-218 promotes apoptosis of U2OS osteosarcoma cells through targeting BIRC5, by D.-Z. Wang, S.-F. Jing, S.-B. Hao, X.-Y. Huang, Q.-T. Miao, J.-F. Gao, published in Eur Rev Med Pharmacol Sci 2018; 22(20): 6650-6657u2013DOI: 10.26355 eurrev_201810_16140u2013PMID: 30402837u201d has been withdrawn. The Publisher apologizes for any inconvenience this may cause. ![file] The paper had been flagged in a Google document as showing [the signs of a papermill provenance] . https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit#gid=0 One feature of this papermill is the frequent disconnection between the name of the nominal corresponding author and the email address provided. ![file] ,
IL-2– and IL-15–induced activation of the rapamycin-sensitive mTORC1 pathway in malignant CD4+ T lymphocytes
Authors: Mariusz A Wasik
Agnieszka Witkiewicz
Monika Kasprzycka
Erle Robertson
Niels Odum
Michal Marzec
Xiaobin Liu
Puthiyaveettil N Raghunath
Mouna El-Salem
Journal: Blood (2008)
Discipline: CLINICAL MEDICINE
Keywords: mTORC1 signaling pathway; CTCL; activation mechanisms; biologic role; PI3K/Akt pathway
Affiliations: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA., Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia;, Department of Pathology, Jefferson Medical College, Philadelphia, PA;, Department of Microbiology, University of Pennsylvania, Philadelphia; and, Institute of Molecular Biology, University of Copenhagen, Copenhagen, Denmark

Abstract:  We examined functional status, activation mechanisms, and biologic role of the mTORC1 signaling pathway in malignant CD4(+) T cells derived from the cutaneous T-cell lymphoma (CTCL). Whereas the spontaneously growing CTCL-derived cell lines displayed persistent activation of the TORC1 as well as the PI3K/Akt and MEK/ERK pathways, the IL-2-dependent cell lines activated the pathways in response to IL-2 and IL-15 but not IL-21. Activation of mTORC1 and MEK/ERK was nutrient dependent. The mTORC1, PI3K/Akt, and MEK/ERK pathways could also be activated by IL-2 in the primary leukemic, mitogen-preactivated CTCL cells. mTORC1 activation was also detected in the CTCL tissues in the lymphoma stage-dependent manner with the highest percentage of positive cells present in the cases with a large cell transformation. Rapamycin inhibited mTORC1 signaling and suppressed CTCL cell proliferation but showed little effect on their apoptotic rate when used as a single agent. Activation of the mTORC1, PI3K/Akt, and MEK/ERK pathways was strictly dependent on the Jak3 and Jak1 kinases. Finally, mTORC1 activation was transduced preferentially through the PI3K/Akt pathway. These findings document the selective gammac-signaling cytokine-mediated activation of the mTORC1 pathway in the CTCL cells and suggest that the pathway represents a therapeutic target in CTCL and, possibly, other T-cell lymphomas. 

Retracted: No

PubPeer comments:
 Figure 1D. Much more similar than you would expect. https: imgur.com Vp8tNT4 , 
 Figure 3A. Much more similar than you would expect. https: imgur.com 9GXMVqo , 
 Figures 4A and 5A. Much more similar than you would expect. https: imgur.com feXiafK , 
 #1 Figure 1D continued. Much more similar after horizontal flip than expected. ![file] ,
Curcumin inhibits tumor growth and angiogenesis in an orthotopic mouse model of human pancreatic cancer
Authors: Sabrina Bimonte
Giuseppe Palma
Antonio Luciano
Domenica Rea
Antonio Barbieri
Claudio Arra
Journal: BioMed Research International (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Pancreatic cancer; gemcitabine; side effects; curcumin; antitumor effects
Affiliations: Istituto Nazionale per lo Studio e la Cura dei Tumori "Fondazione G. Pascale", IRCCS, Via Mariano Semmola, 80131 Naples, Italy., Istituto Nazionale per lo Studio e la Cura dei Tumori “Fondazione G. Pascale”, IRCCS, Via Mariano Semmola, 80131 Naples, Italy, Istituto di Endocrinologia e Oncologia Sperimentale del Consiglio Nazionale delle Ricerche, Dipartimento di Biologia e Patologia Cellulare e Molecolare “L. Califano”, Università degli Studi di Napoli “Federico II”, Via Pansini 5, 80131 Napoli, Italy

Abstract:  Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas. The best chemotherapeutic agent used to treat pancreatic cancer is the gemcitabine. However, gemcitabine treatment is associated with many side effects. Thus novel strategies involving less toxic agents for treatment of pancreatic cancer are necessary. Curcumin is one such agent that inhibits the proliferation and angiogenesis of a wide variety of tumor cells, through the modulation of many cell signalling pathways. In this study, we investigated whether curcumin plays antitumor effects in MIA PaCa-2 cells. In vitro studies showed that curcumin inhibits the proliferation and enhances apoptosis of MIA PaCa-2 cells. To test whether the antitumor activity of curcumin is also observed in vivo, we generated an orthotopic mouse model of pancreatic cancer by injection of MIA PaCa-2 cells in nude mice. We placed mice on diet containing curcumin at 0.6% for 6 weeks. In these treated mice tumors were smaller with respect to controls and showed a downregulation of the transcription nuclear factor NF-κB and NF-κB-regulated gene products. Overall, our data indicate that curcumin has a great potential in treatment of human pancreatic cancer through the modulation of NF-κB pathway. 

Retracted: No

PubPeer comments:
 I would like to ask if the materials in this paper (DOI: 10.1016 j.eurpolymj.2019.01.062) are the exact same, or different, from the paper  Surface modified of polyacrylonitrile nanofibers by TiO2 MWCNT for photodegradation of organic dyes and pharmaceutical drugs under visible light irradiation (DOI: 10.1016 j.envres.2019.108788) I am wondering because the appear to have the exact same photoluminescence spectra for all three materials: ![file] ![file] However, the FTIR spectra are clearly different: ![file] ![file] ,
Co-expression of DevR and DevR(N)-Aph proteins is associated with hypoxic adaptation defect and virulence attenuation of Mycobacterium tuberculosis
Authors: Prahlad Kumar
V D Ramanathan
Jaya Sivaswami Tyagi
Shyamasree De Majumdar
Kohinoor Kaur
V Balasangameshwara
Santosh Chauhan
Vijay K Challu
Deepak Sharma
Atul Vashist
Neetu Kumra Taneja
Journal: PLoS ONE (2010)
Discipline: Multidisciplinary
Keywords: DevR response regulator; hypoxic adaptation; virulence; Mycobacterium tuberculosis; DevR regulon genes
Affiliations: Department of Biotechnology, All India Institute of Medical Sciences, New Delhi, India.

Abstract:  Background: The DevR response regulator is implicated in both hypoxic adaptation and virulence of Mycobacterium tuberculosis (M. tb). DevR regulon genes are powerfully induced in vivo implicating them in bacterial adaptation to host control strategies. A better understanding of DevR function will illumine the way for new strategies to control and treat tuberculosis. Methodology/principal findings: Towards this objective, we used a combination of genetic, microbiological, biochemical, cell biological tools and a guinea pig virulence assay to compare the hypoxic adaptation and virulence properties of two novel M. tb strains, namely, a devR disruption mutant, Mut1, that expresses C-terminal truncated N-terminal domain of DevR (DevR(NTD)) as a fusion protein with AphI (DevR(N)-Kan), and its complemented strain, Comp1, that expresses intact DevR along with DevR(N)-Kan. Comp1 bacteria exhibit a defect in DevR-mediated phosphosignalling, hypoxic induction of HspX and also hypoxic survival. In addition, we find that Comp1 is attenuated in virulence in guinea pigs and shows decreased infectivity of THP-1 cells. While Mut1 bacilli are also defective in hypoxic adaptation and early growth in spleen, they exhibit an overall virulence comparable to that of wild-type bacteria. Conclusions/significance: The hypoxic defect of Comp1 is associated to a defect in DevR expression level. The demonstrated repression of DevR function by DevR(N)-Kan suggests that such a knockdown approach could be useful for evaluating the activity of DevRS and other two-component signaling pathways. Further investigation is necessary to elucidate the mechanism underlying Comp1 attenuation. 

Retracted: No

PubPeer comments:
 Figure 1 appears to have several areas which repeat. *** Inverse image ![file] *** Original ![file] *** Full figure ![file] , 
 A colleague informed us a few days ago about this comment on Figure 1 in our manuscript. We will update our response as soon as we go through the blots and understand how the duplications have happened. We will also write to the journal accordingly. Shyamasree De Majumdar and Jaya S. Tyagi , 
 #2 Thank you for responding here and for planning to correct any errors. , 
 ![file] ,
Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster
Authors: Duonan Yu
Cinzia Sevignani
Michael Dews
Greg H Enders
Andrei Thomas-Tikhonenko
Emma E Furth
Joshua T Mendell
Asal Homayouni
William M Lee
Erik Wentzel
Danielle Murphy
Journal: Nature genetics (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: KRAS; MYC; TP53; VEGF; angiogenic
Affiliations: Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

Abstract:  Human adenocarcinomas commonly harbor mutations in the KRAS and MYC proto-oncogenes and the TP53 tumor suppressor gene. All three genetic lesions are potentially pro-angiogenic, as they sustain production of vascular endothelial growth factor (VEGF). Yet Kras-transformed mouse colonocytes lacking p53 formed indolent, poorly vascularized tumors, whereas additional transduction with a Myc-encoding retrovirus promoted vigorous vascularization and growth. In addition, VEGF levels were unaffected by Myc, but enhanced neovascularization correlated with downregulation of anti-angiogenic thrombospondin-1 (Tsp1) and related proteins, such as connective tissue growth factor (CTGF). Both Tsp1 and CTGF are predicted targets for repression by the miR-17-92 microRNA cluster, which was upregulated in colonocytes coexpressing K-Ras and c-Myc. Indeed, miR-17-92 knockdown with antisense 2'-O-methyl oligoribonucleotides partly restored Tsp1 and CTGF expression; in addition, transduction of Ras-only cells with a miR-17-92-encoding retrovirus reduced Tsp1 and CTGF levels. Notably, miR-17-92-transduced cells formed larger, better-perfused tumors. These findings establish a role for microRNAs in non-cell-autonomous Myc-induced tumor phenotypes. 

Retracted: No

PubPeer comments:
 HU does not refer to heat unstable. Whereas, HU family proteins are highly thermostable. As far as nomenclature HU is concerned; H denotes  Histone like and U refers to  E.coli U93 strain ( Strain from where HU was first isolated). References: https: doi.org 10.1093 nar gkm667 ,
Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4
Authors: A B Di Stefano
A Agrusa
F Iovino
M Perez Alea
M G Francipane
H Walczak
C Di Bernardo
P Cammareri
Y Lombardo
M Todaro
G Stassi
G Condorelli
Journal: Cell death and differentiation (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: mechanisms; resistance; cell death; epithelial cancers; antiapoptotic proteins
Affiliations: Department of Surgical and Oncological Sciences, University of Palermo, Palermo, Italy.

Abstract:  We investigated the mechanisms involved in the resistance to cell death observed in epithelial cancers. Here, we identify that primary epithelial cancer cells from colon, breast and lung carcinomas express high levels of the antiapoptotic proteins PED, cFLIP, Bcl-xL and Bcl-2. These cancer cells produced interleukin-4 (IL-4), which amplified the expression levels of these antiapoptotic proteins and prevented cell death induced upon exposure to TRAIL or other drug agents. IL-4 blockade resulted in a significant decrease in the growth rate of epithelial cancer cells and sensitized them, both in vitro and in vivo, to apoptosis induction by TRAIL and chemotherapy via downregulation of the antiapoptotic factors PED, cFLIP, Bcl-xL and Bcl-2. Furthermore, we provide evidence that exogenous IL-4 was able to upregulate the expression levels of these antiapoptotic proteins and potently stabilized the growth of normal epithelial cells rendering them apoptosis resistant. In conclusion, IL-4 acts as an autocrine survival factor in epithelial cells. Our results indicate that inhibition of IL-4/IL-4R signaling may serve as a novel treatment for epithelial cancers. 

Retracted: No

PubPeer comments:
null, 
null, 
 **Correction to: Cell Death Disease** https: doi.org 10.1038 sj.cdd.4402305 published online 18 January 2018 We have only now noticed (sic) that in Fig. 3a, the immunohistochemical analysis of IL-4Ru03b1 on paraffin-embedded sections from breast is incorrect: IL-4 from breast was duplicated and used for the IL-4Ru03b1 staining. The correct Fig. 3a is given below. ![file] ,
Non-invasive vaccine delivery in transfersomes, niosomes and liposomes: a comparative study
Authors: D P Chatterji
Prem N Gupta
Amit Rawat
Sanyog Jain
Vivek Mishra
Praveen Dubey
Suresh P Vyas
Sunil Mahor
Journal: International Journal of Pharmaceutics (2005)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Non-invasive vaccine delivery; Topical immunization; Vesicular systems; Transfersomes; Niosomes
Affiliations: Drug Delivery Research Laboratory, Department of Pharmaceutical Sciences, Dr. Harisingh Gour University, Sagar 470003, MP, India.

Abstract:  Non-invasive vaccine delivery is a top priority for public health agencies because conventional immunization practices are unsafe and associated with numerous limitations. Recently, the skin has emerged as a potential alternative route for non-invasive delivery of vaccine. Topical immunization (TI), introduction of antigen through topical application onto the intact skin, has many practical merits compared to injectable routes of administration. One of the possibilities for increasing the penetration of bioactives through the skin is the use of vesicular systems. Specially designed lipid vesicles are attracting intense attention and can be used for non-invasive antigen delivery. In the present study, elastic vesicle transfersomes, non-ionic surfactant vesicles (niosomes) and liposomes were used to study their relative potential in non-invasive delivery of tetanus toxoid (TT). Transfersomes, niosomes and liposomes were prepared and characterized for shape, size and entrapment efficiency. These vesicles were extruded through polycarbonate filter (50-nm pore size) to assess the elasticity of the vesicles. The immune stimulating activity of transfersomes, niosomes and liposomes were studied by measuring the serum anti-TT IgG titre following topical immunization. The immune response elicited by topical immunization was compared with that elicited by same dose of alum-adsorbed tetanus toxoid (AATT) given intramuscularly. The results indicate that optimal formulations of transfersomes, niosomes and liposomes could entrap 72.7+/-3.4, 42.5+/-2.4 and 41.3+/-2.2% of antigen and their elasticity values were 124.4+/-4.2, 29.3+/-2.4 and 21.7+/-1.9, respectively. In vivo study revealed that topically given TT containing transfersomes, after secondary immunization, could elicit immune response (anti-TT-IgG) that was equivalent to one that produced following intramuscularly alum-adsorbed TT-based immunization. In comparison to transfersomes, niosomes and liposomes elicited weaker immune response. Thus transfersomes hold promise for effective non-invasive topical delivery of antigen(s). 

Retracted: No

PubPeer comments:
  Fig. 1. Transmission electron microscope (TEM) photomicrograph of ... niosomes (C). I am impressed by the number of duplicate niosomes: ![file] ,
Angelica polysaccharide alleviates oxidative response damage in HaCaT cells through up-regulation of miR-126
Authors: Xijun Zhang
Manqing Qu
Jing Yu
Hong Xue
Pengfei Dai
Ping Zhou
Li Liu
Journal: Experimental and molecular pathology (2019)
Discipline: CLINICAL MEDICINE
Keywords: Angelica polysaccharide (AP); Oxidative damage; Pressure ulcers (PUs); miR-126.
Affiliations: Department of Coronary Care Unit, Qingdao Hiser Medical Center, Qingdao 266033, China., Second Department of Cardiovascular, Qingdao Hiser Medical Center, Qingdao 266003, China., Department of Cadre Health Care, Qingdao Hiser Medical Center, Qingdao 266003, China., Department of Hepatobiliary Internal Medicine, Qingdao Hiser Medical Center, Qingdao 266003, China.. Electronic address: .

Abstract:  Background: Pressure ulcers (PUs) prevalence has been considered as an index for patient safety and cure quality of hospital and community. Skin cellular oxidative response damage is existed in the development of PUs. Angelica polysaccharide (AP) has the anti-oxidation function. Therefore, our goal was to investigate the mechanism of AP in relieving cellular oxidative damage. Methods: Transfected HaCaT cells with miR-126 inhibitor, pre-treated by AP, and then treated by H2O2. CCK-8 assay and flow cytometry detection were set to test viability and apoptosis of cells respectively. qRT-PCR and western blot tested levels of miR-126 and oxidative damage relative factors. ROS assay tested the production of ROS in cells. Results: Cellular oxidative response damage was induced by H2O2 at concentration of 300 μM. We found that AP could attenuate cellular oxidative response damage caused by H2O2 that it elevated cell viability, attenuated cell apoptosis and production of ROS and promoted activation of PI3K/AKT and mTOR signal pathways. Further, miR-126 was up-regulated by AP. The up-regulation of miR-126 could activate the PI3K/AKT and mTOR signal pathways. Conclusion: Our study demonstrated that AP attenuated cellular oxidative response damage in HaCaT cells by positively regulated miR-126. 

Retracted: Yes

PubPeer comments:
 Reference [1] is [1] Abdullatif AA, Abdullatif FA, Safar AA (2019) Multi -focus image fusion based on stationary wavelet transform and PCA on YCBCR color space. Journal of Southwest Jiaotong University 54(5). This is published in a [hijacked] [version] of JSJU ([hijacker website](http: www.jsju.org index.php journal) [authentic website](http: journal16.magtechjournal.com Jweb_xnjd CN volumn current.shtml)). Has the author vetted the credibility of this reference? Springer s [policy] on predatory sources may be of relevance. ,