PReD-Bench/PRed-Bench huggingface dataset:
Anti-neuronal autoantibodies: Current diagnostic challenges
Authors: Lars Komorowski
Winfried Stoecker
Sandra Saschenbrecker
Christian Probst
Journal: Multiple sclerosis and related disorders (2014)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Anti-neuronal autoantibodies; Biochip mosaic; Indirect immunofluorescence test; Inducible cell line; Marker protein
Affiliations: Institute for Experimental Immunology, Euroimmun, Luebeck, Germany. Electronic address: ., Institute for Experimental Immunology, Euroimmun, Luebeck, Germany.

Abstract:  The spectrum of neurological autoimmune diseases has expanded substantially in the last 15 years due to the discovery of new anti-neuronal antibodies. There are at present numerous technical challenges for developing and improving standardized serological test systems for the detection of these autoantibodies, some of which occur very rarely. In particular, the determination of autoantibodies against complex cell surface structures generally requires authentically presented target antigens. Finally, research into syndrome associations benefits from multiplex analyses and accelerates the understanding of the complex autoimmune processes, forming an important basis for the development of novel therapy concepts. 

Retracted: No

PubPeer comments:
 Figure 1 shows Biochip slides, which are covered with cells expressing peptides and incubated with patient sera. Panels in A, B, and C, represents three different patients. As shown with rectangles of the same color, some of the panels look very similar to each other, albeit sometimes zoomed in differently, or rotated. Could the authors please explain what happened here? ![file] ,
Suppressive effect of microRNA-138 on the proliferation and invasion of osteosarcoma cells via targeting SIRT1
Authors: Hao Mo
Ligen Mo
Xiang Lin
Juliang He
Zhenjie Wu
Zhenchao Yuan
Journal: Experimental and therapeutic medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: invasion; microRNA-138; osteosarcoma; proliferation; sirtuin 1.
Affiliations: Department of Bone and Soft Tissue Neurosurgery, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

Abstract:  MicroRNAs (miRs), a class of small non-coding RNAs, function as key regulators in gene expression through binding to the 3'-untranslated region (UTR) of their target mRNA, which further leads to translational repression or mRNA degradation. Recently, miR-138 has been found to have a tumor suppressive role in a variety of human malignancies. However, the exact role of miR-138 in regulating the malignant phenotypes of osteosarcoma (OS) has remained to be elucidated. In the present study, reverse-transcription PCR analysis showed that the expression of miR-138 was markedly reduced in OS tissues compared to that in matched adjacent non-tumorous tissues. Furthermore, it was also downregulated in several common OS cell lines, when compared with that in a normal human osteoblast cell line. Overexpression of miR-138 suppressed cell proliferation and invasion and led to a significant decrease in the protein expression of sirtuin 1 (SIRT1), which was further identified as a direct target gene of miR-138 in MG63 cells. Moreover, restoration of SIRT1 expression reversed the suppressive effects of miR-138 on MG63 cell proliferation and invasion. Finally, the expression of SIRT1 was found to be significantly upregulated in OS tissues compared to that in matched adjacent tissues, and SIRT1 levels were inversely correlated with the miR-138 levels in OS tissues. Therefore, the present study demonstrated that miR-138 has a role in inhibiting OS cell proliferation and invasion via directly targeting SIRT1, and suggested that the miR-138/SIRT1 axis may become a promising therapeutic target for OS. 

Retracted: No

PubPeer comments:
 Figs 2D, 4D. ![] Compare Figs 3D, 4D, 5B, 5F from [Dang et al (2017)] . ![] Figures 2C, 4C from [Zhou et al (2017)] . ![] . ,
Cross-regulation of C/EBP alpha and PPAR gamma controls the transcriptional pathway of adipogenesis and insulin sensitivity
Authors: A E Troy
B M Spiegelman
G J Darlington
G Adelmant
S Hauser
C McKeon
R Brun
E D Rosen
Z Wu
Journal: Molecular cell (1999)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: C/EBP alpha; adipose tissue development; PPAR gamma; adipose differentiation; lipid accumulation
Affiliations: Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

Abstract:  Mice deficient in C/EBP alpha have defective development of adipose tissue, but the precise role of C/EBP alpha has not been defined. Fibroblasts from C/EBP alpha(-/-) mice undergo adipose differentiation through expression and activation of PPAR gamma, though several clear defects are apparent. C/EBP alpha-deficient adipocytes accumulates less lipid, and they do not induce endogenous PPAR gamma, indicating that cross-regulation between C/EBP alpha and PPAR gamma is important in maintaining the differentiated state. The cells also show a complete absence of insulin-stimulated glucose transport, secondary to reduced gene expression and tyrosine phosphorylation for the insulin receptor and IRS-1. These results define multiple roles for C/EBP alpha in adipogenesis and show that cross-regulation between PPAR gamma and C/EBP alpha is a key component of the transcriptional control of this cell lineage. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
null, 
 Another possible issue appears when you compare Fig. 3 with Fig. 4A. It looks like 36B4 bands are the same (horizontally inverted), while the experimental conditions should be different. Could authors provide an explanation? ![file] ,
Downregulation of uPAR and cathepsin B induces apoptosis via regulation of Bcl-2 and Bax and inhibition of the PI3K/Akt pathway in gliomas
Authors: Jasti S Rao
Sanjeeva Mohanam
Christopher S Gondi
Sreelatha Gopinath
Meena Gujrati
Kiranmai Alapati
Ramarao Malla
Dzung H Dinh
Journal: PloS one (2010)
Discipline: Multidisciplinary
Keywords: Glioma; uPAR; cathepsin B; apoptosis; caspase
Affiliations: Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, Illinois, United States of America.

Abstract:  Background: Glioma is the most commonly diagnosed primary brain tumor and is characterized by invasive and infiltrative behavior. uPAR and cathepsin B are known to be overexpressed in high-grade gliomas and are strongly correlated with invasive cancer phenotypes. Methodology/principal findings: In the present study, we observed that simultaneous downregulation of uPAR and cathepsin B induces upregulation of some pro-apoptotic genes and suppression of anti-apoptotic genes in human glioma cells. uPAR and cathepsin B (pCU)-downregulated cells exhibited decreases in the Bcl-2/Bax ratio and initiated the collapse of mitochondrial membrane potential. We also observed that the broad caspase inhibitor, Z-Asp-2, 6-dichlorobenzoylmethylketone rescued pCU-induced apoptosis in U251 cells but not in 5310 cells. Immunoblot analysis of caspase-9 immunoprecipitates for Apaf-1 showed that uPAR and cathepsin B knockdown activated apoptosome complex formation in U251 cells. Downregulation of uPAR and cathepsin B also retarded nuclear translocation and interfered with DNA binding activity of CREB in both U251 and 5310 cells. Further western blotting analysis demonstrated that downregulation of uPAR and cathepsin B significantly decreased expression of the signaling molecules p-PDGFR-β, p-PI3K and p-Akt. An increase in the number of TUNEL-positive cells, increased Bax expression, and decreased Bcl-2 expression in nude mice brain tumor sections and brain tissue lysates confirm our in vitro results. Conclusions/significance: In conclusion, RNAi-mediated downregulation of uPAR and cathepsin B initiates caspase-dependent mitochondrial apoptosis in U251 cells and caspase-independent mitochondrial apoptosis in 5310 cells. Thus, targeting uPAR and cathepsin B-mediated signaling using siRNA may serve as a novel therapeutic strategy for the treatment of gliomas. 

Retracted: Yes

PubPeer comments:
 Unfortunately, Figures 3A and 3B in this article by Weimin et al. are the exact copy of Figures 2D and 2F, respectively from a Cancer Discovery article of August 22, 2017; DOI: 10.1158 2159-8290.CD-17-0538. These figures belong to a different construct project by different authors. ,
Retracted : MicroRNA‐497 accelerates apoptosis while inhibiting proliferation, migration, and invasion through negative regulation of the MAPK/ERK signaling pathway via RAF‐1
Authors: Qi Zhou
Ling Tao
Chun-Yu Zhang
Lei Guo
Na-Na Han
Zhi-Le Liu
Xia Li
Journal: Journal of Cellular Physiology (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RAF-1; apoptosis; cervical cancer; extracellular; microRNA-497
Affiliations: The 4th Department of Gynecological Surgery Affiliated Tumor Hospital of Xinjiang Medical University  Urumqi P.R. China, Department of Oncology The First Affiliated Hospital of Kunming Medical University  Kunming P.R. China

Abstract:  The aim of this study is to explore the various modes of action miR-497 has on human cervical cancer (CC) cell behavior. We also speculate that miR-497 achieves its anti-tumor role by governing RAF-1 via MAPK/ERK signaling pathway. CC tissues with corresponding adjacent normal tissues were collected from 168 CC patients. RAF-1-positive cells were identified by means of immunohistochemistry in tissues. A series of inhibitors, mimics and siRNA against RAF-1 were introduced to validate regulatory mechanisms for miR-497 and RAF-1. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay were employed for evaluating alternations of miR-497, RAF-1, and MAPK/ERK signaling pathway. HeLa cell proliferation, invasion, migration, cycle progression, and apoptosis were assessed by means of CCK-8, wound-healing, transwell invasion assays, and flow cytometry, respectively. The target prediction program and luciferase activity determination were used to identify miR-497 targeting RAF-1. We determined reduced miR-497 expression and elevated expression of RAF-1 in CC tissues as opposed to adjacent tissues. Transfection of miR-497 mimics and siRNA-RAF-1 both decreased levels of MEK1, ERK1, and p38 phosphorylation in HeLa cells, inhibited cell proliferation, migration and invasion, induced more cells arrested in the G0/G1 phase, and promoted cell apoptosis; while miR-497 inhibitors led to opposite results. These findings indicate miR-497 as a tumor suppressor results from negative regulation of the MAPK/ERK signaling pathway via RAF-1 in CC. 

Retracted: Yes

PubPeer comments:
 Fig 2C (at left). At right, Fig 6H from [Zhang et al (2018)] . Unexpected similarity between the RAF-1 and E-cadherin bands respectively (after a horizontal flip and vertical rescaling). ![file] More generally, the WBs in this paper seem to come from a confined gamut of protein-blob shapes shared across a number of papers from different authors, as in this montage: ![] , 
 Retracted [1 July 2021] . ---------------------------- The above article, published online on 21 December 2017 in Wiley Online Library has been retracted by agreement between the authors, journal s Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. ,
VAMP-associated protein B (VAPB) promotes breast tumor growth by modulation of Akt activity
Authors: David Greenstein
Aixiang Jiang
Dana Brantley-Sieders
Jin Chen
Wenqiang Song
Sima Lev
Meghana Rao
Yu Shyr
Journal: PLoS ONE (2012)
Discipline: Multidisciplinary
Keywords: VAPB; breast cancer; tumor cells; proliferation; AKT activation
Affiliations: Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America.

Abstract:  VAPB (VAMP- associated protein B) is an ER protein that regulates multiple biological functions. Although aberrant expression of VAPB is associated with breast cancer, its function in tumor cells is poorly understood. In this report, we provide evidence that VAPB regulates breast tumor cell proliferation and AKT activation. VAPB protein expression is elevated in primary and metastatic tumor specimens, and VAPB mRNA expression levels correlated negatively with patient survival in two large breast tumor datasets. Overexpression of VAPB in mammary epithelial cells increased cell growth, whereas VAPB knockdown in tumor cells inhibited cell proliferation in vitro and suppressed tumor growth in orthotopic mammary gland allografts. The growth regulation of mammary tumor cells controlled by VAPB appears to be mediated, at least in part, by modulation of AKT activity. Overexpression of VAPB in MCF10A-HER2 cells enhances phosphorylation of AKT. In contrast, knockdown of VAPB in MMTV-Neu tumor cells inhibited pAKT levels. Pharmacological inhibition of AKT significantly reduced three-dimensional spheroid growth induced by VAPB. Collectively, the genetic, functional and mechanistic analyses suggest a role of VAPB in tumor promotion in human breast cancer. 

Retracted: No

PubPeer comments:
 ![file] , 
 In Fig. 4C of this paper, the same cells are used for two microscopy fields but are labelled up differently. ![image] , 
 Thank you for spotting this and bringing it to our attention. We will locate the original stained slides and replace the duplicated image. You do great work, and we appreciate it! - Dana Brantley-Sieders, Vanderbilt University Medical Center , 
 We will also contact PLoS ONE to replace the image! , 
 Update - we have contacted PLoS One with the correction. Once more, we thank you for bringing this to our attention. ![file] , 
 Update - received a reply from PLoS One acknowledging request to update. Will post with any additional updates. ,
Retracted: Transketolase A, an enzyme in central metabolism, derepresses themarRABmultiple antibiotic resistance operon ofEscherichia coliby interaction with MarR
Authors: Xiaowen R Bina
Francis Domain
Stuart B Levy
Journal: Molecular Microbiology (2007)
Discipline: MICROBIOLOGY
Keywords: Escherichia coli; marRAB operon; regulatory proteins; MarR; MarA

Abstract:  The Escherichia coli marRAB operon specifies two regulatory proteins, MarR (which represses) and MarA (which activates expression of the operon). The latter controls expression of multiple other chromosomal genes implicated in cell physiology, multiple drug resistance and virulence. Using randomly cloned E. coli DNA fragments in the bacterial adenylate cyclase two-hybrid system, we found that transketolase A (TktA) interacts with MarR. Purified (6H)-TktA immobilized on NiNTA resin-bound MarR. Overexpression or deletion of tktA showed that TktA interfered with MarR repression of the marRAB operon. Deletion of tktA increased antibiotic and oxidative stress susceptibilities, while its overexpression decreased them. Hydrogen peroxide induced tktA at 1 h treatment, while an increase in marRAB expression occurred only after 3 h exposure. This increase was dependent on the presence of tktA. Two MarR mutations which eliminated MarR binding to the marRAB operator and one which decreased dimerization of MarR had no effect on MarR interaction with TktA in the two-hybrid system. However, the interaction was disrupted by one of the three tested superrepressor mutant MarR proteins known to increase MarR binding to DNA. TktA inhibition of repression by MarR demonstrates a previously unrecognized level of control of the expression of marRAB operon. 

Retracted: No

PubPeer comments:
 I am the corresponding author of this article. In searching for the earlier mistakes in our lab, today I found a duplicated image for the DNA sequencing of BRAF gene we mistakenly used (Fig 1D and E, normal). Actually, it is the normal sequence and is not different according to the SSCP, it should have not been used twice. Although the mistake might not alter the study conclusion, we would like to confirm that it was used. I feel sorry that we including the 1st author and corresponding author did not check the images carefully. ![file] ,
miR-153-3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene
Authors: Yuchun Song
Shoubin Cui
Wei Zhao
Cui Li
Yinmin Zhang
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MCL1; miR-153-3p; ovarian carcinoma; tumor growth.
Affiliations: Department of Gynaecology and Obstetrics, Yantai Affiliated Hospital, Binzhou Medical College, Yantai, Shandong, China., Department of Gynaecology, The People's Hospital of Rizhao, Rizhao, Shandong, China., Department of Reproduction, Dezhou People's Hospital, Dezhou, Shandong, China., Department of Gynaecology, Yantai Affiliated Hospital, Binzhou Medical College, Yantai, Shandong, China.

Abstract:  The study of either miR-153-3p or MCL1 gene in ovarian carcinoma (OVC) has been reported; however, the interaction between miR-153-3p and MCL1 gene in OVC as well as the influence of their interaction on OVC progression has not been reported yet. Herein we intended to study the effects of miR-153-3p/MCL1 axis in OVC. Web-based bioinformatics algorithms including DIANA TarBase 8.0, PicTar, and TargetScan Human 7.2 were used to predict the microRNAs (miRNAs) that could target MCL1 mRNA. Patient characteristics data collection and tissue sample immunohistochemical staining were used to determine the expression level of miR-153-3p and MCL1. We determined to unravel the effects of the pairing-up of miR-153-3p and MCL1 mRNA in OVC cell lines (OVCAR3 cell line and A2780) and xenografts (immunodeficient(immunodeficient Rag-/- mice) using several methods including real-time quantitative reverse transcription polymerase chain reaction, westernWestern blot, colony formation assay, wound healing assay, Transwell invasion assay, flow cytometry assay, and xenograft assay. These experiments were performed to study OVC cellular activities such as cell growth and death and so forth in vitro and in vivo. Plenty of miRNAs that can target MCL1 mRNA have been identified, and we have narrowed them down to miR-153-3p. MCL1 gene was found overexpressed in OVC tissues and OVC cell lines at RNA and protein levels, whereas miR-153-3p was found under-expressed in OVC tissues and cells. miR-153-3p was found to target MCL1 mRNA and interfered OVC progression. The repression of MCL1 gene expression caused by either miR-153-3p or small interfering RNA technique led to significantly reduced OVC cell growth and invasion in vitro. Lastly, the engraftment of transfected human OVC cells into Rag-/- mice confirmed the in vitro results. MCL1 gene acts as a cancer facilitator in OVC. In this study, we revealed the role of miR-153-3p on OVC progression by targeting MCL1 gene. Our work could comprehend the current understanding of OVC progression and contribute to the underlying aggression mechanism of this cancer. 

Retracted: No

PubPeer comments:
 In Figure 4B: microscopy data has been duplicated and presented as something else. In Figure 5C: microscopy data has been duplicated and presented as something else. ![file] ,
MiR-1301-3p inhibits human breast cancer cell proliferation by regulating cell cycle progression and apoptosis through directly targeting ICT1
Authors: Xiang Peng
Yufeng Shen
Bin Yan
Journal: Breast Cancer (2018)
Discipline: CLINICAL MEDICINE
Keywords: Apoptosis; Breast cancer; Cell cycle; Cell proliferation; ICT1
Affiliations: Department of Surgery, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Shanghai, 201700, China., Department of Surgery, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Shanghai, 201700, China. .

Abstract:  Background: MiRNAs regulate a variety of biological processes, such as cell proliferation and apoptosis and play critical roles in cancer progression. Accumulating studies have demonstrated that miR-1301-3p could regulate the development and progression of multiple cancers, but its biological behaviors in breast cancer (BC) are still elusive. Methods: The expression of miR-1301-3p was determined in BC tissues and cell lines using quantitative real-time PCR analysis. The effects of miR-1301-3p on BC cell growth, proliferation, cell cycle distribution, and apoptosis were also explored in vitro using MTT, colony formation and Flow cytometry assays. The potential target gene of miR-1301-3p was determined by dual-luciferase reporter assay and verified by quantitative real-time PCR and western blot analysis. Results: We found the expression of miR-1301-3p was observably significantly down-regulated in BC tissues and cell lines. MiR-1301-3p expression in BC tissues was significantly associated with tumor size and clinical stage. Gain-of-function assays demonstrated that miR-1301-3p inhibited the cell growth and proliferation in breast cancer cell lines, MCF-7 and T-47D. Moreover, up-regulation of miR-1301-3p induced cell cycle G0/G1 phase arrest and apoptosis. Mechanistically, up-regulation of miR-1301-3p reduced the expression of CDK4, Cyclin D1, Bcl-2, but elevated the expression of p21, Bad and Bax. ICT1 was confirmed as a direct target of miR-1301-3p. Furthermore, ICT1 overexpression could partially reverse the effects of miR-1301-3p on BC cell proliferation, cell cycle progression and apoptosis. Conclusion: Our observations suggested that miR-1301-3p inhibits cell proliferation via inducing cell cycle arrest and apoptosis through targeting ICT1, and might be a therapeutic target for BC. 

Retracted: No

PubPeer comments:
 Extremely similar blot bands found in 2 figures for different samples and different blots. ![file] , 
 Extremely similar blot bands found in 3 figure panels for different samples and different proteins ![file] ,
Electroacupuncture attenuates cervical spinal cord injury following cerebral ischemia/reperfusion in stroke-prone renovascular hypertensive rats
Authors: Minhua Gu
Yanping Li
Xuewen Wang
Jie Chen
DI Meng
Feng Tan
Yangui Liang
Journal: Experimental and Therapeutic Medicine (2014)
Discipline: CLINICAL MEDICINE
Keywords: cerebral ischemia; cervical spinal cord; neuron; stroke-prone renovascular hypertensive rats.
Affiliations: Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Foshan, Guangdong 528000, P.R. China., Department of Chinese Medicine, Dongsheng Hospital, Guangzhou, Guangdong 510120, P.R. China.

Abstract:  Cerebral ischemia induces injury, not only in the ischemic core and surrounding penumbra tissues, but also in remote areas such as the cervical spinal cord. The aim of the present study was to determine the effects of electroacupuncture (EA) on cervical spinal cord injury following cerebral ischemia/reperfusion in stroke-prone renovascular hypertensive (RHRSP) rats. The results demonstrated that neuronal loss, which was assayed by Nissl staining in the cervical spinal cords of RHRSP rats subjected to transient middle cerebral artery occlusion (MCAO), was markedly decreased by EA stimulation at the GV20 (Baihui) and GV14 (Dazhui) acupoints compared with that in rats undergoing sham stimulation. Quantitative polymerase chain reaction and western blot analysis demonstrated that EA stimulation blocked the MCAO-induced elevated protein expression levels of glial fibrillary acidic protein and amyloid precursor protein in the cervical spinal cord at days 24 and 48. To further investigate the mechanism underlying the neuroprotective role of EA stimulation, the protein expression levels of Nogo-A and Nogo-66 receptor-1 (NgR1), two key regulatory molecules for neurite growth, were recorded in each group. The results revealed that EA stimulation reduced the MCAO-induced elevation of Nogo-A and NgR1 protein levels at day 14 and 28 in RHRSP rats. Therefore, the results demonstrated that EA reduced cervical spinal cord injury following cerebral ischemia in RHRSP rats, indicating that EA has the potential to be developed as a therapeutic treatment agent for cervical spinal cord injury following stroke. 

Retracted: No

PubPeer comments:
 multiple duplications and edits ![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. ,
Proliferative suppression by CDK4/6 inhibition: complex function of the retinoblastoma pathway in liver tissue and hepatoma cells
Authors: Xavier Graña
Christopher N Mayhew
Chellappagounder Thangavel
Dayana B Rivadeneira
Erik S Knudsen
Christopher A Reed
Elena Sotillo
Journal: Gastroenterology (2010)
Discipline: CLINICAL MEDICINE
Keywords: Hepatocellular carcinoma; chemotherapeutic interventions; retinoblastoma tumor suppressor; CDK4/6 inhibition; hepatocyte proliferation
Affiliations: Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Abstract:  Background &amp; aims: Hepatocellular carcinoma is the third leading cause of cancer mortality worldwide; current chemotherapeutic interventions for this disease are largely ineffective. The retinoblastoma tumor suppressor (RB) is functionally inactivated at relatively high frequency in hepatocellular carcinoma and hepatoma cell lines. Here, we analyzed the ability of CDK4/6 inhibition to inhibit hepatocyte proliferation and the effect of RB status on this process. Methods: Hepatoma cell lines and xenograft models harboring RB knockdown and mice harboring liver-specific Rb deletion were used to define the role of RB function in response to CDK4/6 inhibition. Results: Our study shows that CDK4/6-dependent cell cycle progression in hepatoma cells was readily arrested by inhibition of CDK4/6 by PD-0332991 or p16ink4a irrespective of RB status. Interestingly, upon CDK4/6 inhibition, p107 protein stability was dramatically increased as a function of RB loss. This engagement of compensatory mechanisms was critical for cell cycle inhibition in the absence of RB, because both the E1A oncoprotein and overexpression of E2F proteins were capable of overcoming the effect of CDK4/6 inhibition. These findings were recapitulated in xenograft models. Furthermore, to determine how these findings relate to hepatocyte proliferation in vivo, mice were exposed to carbon tetrachloride to induce liver regeneration followed by treatment with PD-0332991. This treatment significantly inhibited hepatocyte proliferation. Strikingly, this facet of PD-0332991 function was retained even in RB-deficient livers. Conclusions: These data show that CDK4/6 inhibition is a potent mediator of cytostasis and that RB loss can be readily compensated for in the context of both hepatoma cell lines and liver tissue. 

Retracted: No

PubPeer comments:
 ![file] , 
 Thank you for pointing this out, I have contacted the journal for a correction. ,
Stem cell membrane-coated isotretinoin for acne treatment
Authors: Shiyi Wang
Jinlan Jiang
Fuqiang Zhang
Rihua Jiang
Mingji Zhu
Yongri Jin
JeungHoon Lee
Jing Li
Tianqi Meng
Journal: Journal of nanobiotechnology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Acne; Isotretinoin; Nanoparticles; Stem cell; Transdermal.
Affiliations: Department of Dermatology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Scientific Research Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., College of Chemistry, Jilin University, Changchun, Jilin, China., Department of Dermatology, School of Medicine, Chungnam National University, Daejeon, Republic of Korea., Department of Dermatology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China. ., Scientific Research Center, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China. .

Abstract:  Background: Topical isotretinoin is commonly used to treat acne. However, topical isotretinoin has side effects and can hardly permeate through the stratum corneum, the most important skin barrier. Therefore, this study aimed to demonstrate the efficacy of nanoparticles as stable carriers with great curative effects, low side effects, and strong transdermal ability. Results: In a rabbit model of hyperkeratinization, STCM-ATRA-NPs showed significant therapeutic efficacy. By contrast, negative therapeutic efficacy was observed in a golden hamster model of hyper sebum production. Scanning electron microscopy and Fourier transform infrared spectral analyses showed that nanoparticles could penetrate the stratum corneum. Western blotting demonstrated that the nanoparticles could enhance the transdermal efficacy of isotretinoin by reducing the effect of keratin and tight junction proteins. Further, nanoparticles enhanced endocytosis, thereby promoting drug penetration and absorption into the skin. Conclusion: STCM-ATRA-NPs were demonstrated to control isotretinoin release, reducing its side effects, and efficiently permeating through the skin by reducing the effect of keratin and tight junction proteins and enhancing endocytosis. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have two images which overlap, with differing dimensions, representing different treatments. *** ![file] , 
 Seems to be a similar issue with Figure 4. *** ![file] , 
 Seems to be a similar issue with Figure 7, with different brightness or contrast. *** ![file] , 
 August 6, 2021  Following publication of our article the authors (sic) found that some of the images in the publication had been misused, so that three images presented at high magnification did not correspond to those at low magnification. The correct images for Figure 3b, Figure 4 (Treatment efficiency on hyper keratinization model by H E stainingu2014Group Blank H Eu00d740) and Figure 7a are shown below. These errors do not affect the conclusions of the work. The authors apologize for these errors and any inconvenience caused. *** ![file] *** ![file] *** Quite a coincidence that the authors found the exact issues I previously reported on PubPeer. ,
BATF2 prevents glioblastoma multiforme progression by inhibiting recruitment of myeloid-derived suppressor cells
Authors: Qiang Luo
Yi Liu
Hantao Zhang
Chunlei Li
Lin Cheng
Jie Deng
Shuang Zhang
Lei Zheng
Qian Xie
Hongxin Deng
Lei Dai
Xun Hu
Dechao Yu
Yang Yang
Qiyong Gong
Xin Zhang
Xiaolan Su
Qingnan Wang
Yi Lin
Ping Fan
Gang Shi
Journal: Oncogene (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: BATF2; extracellular vesicles; glioma growth; myeloid-derived suppressor cells; chemotaxis
Affiliations: State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China., Huaxi MR Research Center, Department of Radiology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China., General Practice Department of West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China., Huaxi Biobank, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China., Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, PR China., Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, PR China. ., State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, Sichuan, PR China. .

Abstract:  The basic leucine zipper ATF-like transcription factor 2 (BATF2) has been implicated in inflammatory responses and anti-tumour effects. Little, however, is known regarding its extracellular role in maintaining a non-supportive cancer microenvironment. Here, we show that BATF2 inhibits glioma growth and myeloid-derived suppressor cells (MDSCs) recruitment. Interestingly, extracellular vesicles (EVs) from BATF2-overexpressing glioma cell lines (BATF2-EVs) inhibited MDSCs chemotaxis in vitro. Moreover, BATF2 inhibited intracellular SDF-1α and contributes to decreased SDF-1α in EVs. In addition, BATF2 downregulation-induced MDSCs recruitment were reversed by blocking SDF-1α/CXCR4 signalling upon AMD3100 treatment. Specifically, detection of EVs in 24 pairs of gliomas and healthy donors at different stages revealed that the abundance of BATF2-positive EVs in plasma (BATF2+ plEVs) can distinguish stage III-IV glioma from stage I-II glioma and healthy donors. Taken together, our study identified novel regulatory functions of BATF2 in regulating MDSCs recruitment, providing a prognostic value in terms of the number of BATF2+ plEVs in glioma stage. 

Retracted: No

PubPeer comments:
 ![file] FIG 4E. The authors should check the original data and make an explanation. ,
Transferrin receptor-targeted HMSN for sorafenib delivery in refractory differentiated thyroid cancer therapy
Authors: You Ke
Cheng Xiang
Journal: International journal of nanomedicine (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: RAF/MEK/ERK; RAI-refractory DTC; hollow mesoporous silica nanoparticles; sorafenib; transferrin.
Affiliations: Department of Nephrology, The Second Affiliated Hospital of Zhejiang University, Hangzhou, China.

Abstract:  Background: Thyroid cancer becomes the most common endocrine cancer with the greatest growing incidence in this decade. Sorafenib is a multikinase inhibitor for the treatment of progressive radioactive iodine-refractory differentiated thyroid cancer (DTC), while the off-target toxicity effect is usually inconvenient for patients taking. Methods: In this study, hollow mesoporous silica nanoparticles (HMSNs) with transferrin modification (Tf-HMSNs) were loaded with sorafenib (sora@Tf-HMSNs) to help targeted delivery of sorafenib. Due to the biocompatible Tf shell, Tf-HMSNs exhibited excellent bio-compatibility and increased intracellular accumulation, which improved the targeting capability to cancer cells in vitro and in vivo. Results: Sora@Tf-HMSNs treatment exhibited the strongest inhibition effect of res-TPC-1 cells and res-BCPAP cells compared with sora@HMSNs and sorafenib groups and induced more cancer cell apoptosis. Finally, Western blot analysis was conducted to check the expression of RAF/MEK/ERK signaling pathway after sorafenib encapsulated Tf-HMSNs treatment. Conclusion: Overall, sora@Tf-HMSNs can significantly increase the effective drug concentration in cancer cells and thus enhance the anticancer effect, which are expected to be promising nanocarriers to deliver anticancer drugs for effective and safe therapy for RAI-refractory DTC. 

Retracted: No

PubPeer comments:
 ![file] ,
Cyclin-dependent kinase 4 expression is essential for neu-induced breast tumorigenesis
Authors: Judith Litvin
Xavier Graña
Richard V Mettus
E Premkumar Reddy
Sushil G Rane
Haritha K D L Reddy
Journal: Cancer Research (2005)
Discipline: CLINICAL MEDICINE
Keywords: cyclin D1; Cdk4; breast tumorigenesis; mice; oncogenes
Affiliations: Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.

Abstract:  Previous work has shown that cyclin D1 expression is required for neu- and ras-induced, but not wnt- or c-myc-induced, breast tumorigenesis in mice. Although cyclin D1 binds and activates cyclin-dependent kinase 4 (Cdk4), thereby mediating activation of a program of E2F-dependent gene expression, it has been suggested that the oncogenic activities of cyclin D1 are independent of Cdk4. To determine whether Cdk4 expression is required for breast tumorigenesis in mice, we have generated compound mice ectopically expressing the neu or wnt oncogenes in the mammary glands of wild-type and Cdk4-/- mice. Our results show that Cdk4 expression is required for efficient neu-induced tumorigenesis but is dispensable for wnt-induced breast tumorigenesis. In contrast to results previously observed in the mammary glands of cyclin D1-/- virgin females, our results show defects in mammary gland development in Cdk4-/- virgin females, suggesting differences in compensatory mechanisms in the absence of either subunit of the cyclin D1/Cdk4 complex. These results suggest that drugs targeted to inhibit Cdk4 activities could be developed to specifically treat certain breast tumors as Cdk4 is not essential for viability. 

Retracted: No

PubPeer comments:
 Figure 4B. https: imgur.com UNkePTG ,
Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma
Authors: Zhao Ma
Ning Chen
Yi Su
Guigang Yan
Lianzhi Yu
Journal: Cell structure and function (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LINC00202; RIN1; miR-3619-5p; progression; retinoblastoma.
Affiliations: Department of Ophthalmology, the Affiliated Yantai Yuhuangding Hospital of Qingdao University., Department of Radiation Oncology, the Affiliated Yantai Yuhuangding Hospital of Qingdao University., Department of Physical Examination, the Affiliated Yantai Yuhuangding Hospital of Qingdao University.

Abstract:  Retinoblastoma (RB) is the most common intraocular malignancy in childhood, and the prognosis in the advanced RB is poor. It is urgent to find novel therapeutic targets. Long noncoding RNAs (lncRNAs) have critical functions in cancer progression, and lncRNA LINC00202 is found associated with poor prognosis in RB. However, the functions of LINC00202 in RB remain unclear. We employed qRT-PCR and immunoblot to detect the expression levels of mRNAs and proteins, respectively. Cell proliferation was determined by CCK-8 assay and colony formation assay. Transwell assays were applied to evaluate the cell abilities of migration and invasion. Luciferase reporter assay was applied to examine RNA stability, and RNA pulldown assays were used to detect interaction between lncRNA and microRNA (miRNA). LINC00202 expression in RB tissues is higher than that in the paired adjacent normal tissues, which has correlation with poor prognosis in RB. RB cell proliferation, migration and invasion were weakened by LINC00202 depletion, but enhanced by LINC00202 overexpression. MiR-3619-5p was identified to directly bind and mediate LINC00202-promoted RB progression, meanwhile, miR-3619-5p directly regulated expression of an oncongene, RIN1. Moreover, RIN1 knockdown completely blocked miR-3619-5p-enhanced RB progression. In summary, high LINC00202 levels are correlated with poor prognosis in RB, and it promotes RB progression by sponging miR-3619-5p and therefore up-regulating RIN1 expression.Key words: LINC00202, miR-3619-5p, retinoblastoma, progression, RIN1. 

Retracted: No

PubPeer comments:
 Fig 4(e,f). The authors may wish to check. ![file] ,
Roles of the troponin isoforms during indirect flight muscle development in Drosophila
Authors: Prabodh Kumar
Upendra Nongthomba
Nallur B Ramachandra
Salam Herojeet Singh
Journal: Journal of Genetics (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Troponin proteins; tropomyosin; striated muscles; contraction; calcium concentration
Affiliations: Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore 560 012, India. .

Abstract:  Troponin proteins in cooperative interaction with tropomyosin are responsible for controlling the contraction of the striated muscles in response to changes in the intracellular calcium concentration. Contractility of the muscle is determined by the constituent protein isoforms, and the isoforms can switch over from one form to another depending on physiological demands and pathological conditions. In Drosophila, amajority of themyofibrillar proteins in the indirect flight muscles (IFMs) undergo post-transcriptional and post-translational isoform changes during pupal to adult metamorphosis to meet the high energy and mechanical demands of flight. Using a newly generated Gal4 strain (UH3-Gal4) which is expressed exclusively in the IFMs, during later stages of development, we have looked at the developmental and functional importance of each of the troponin subunits (troponin-I, troponin-T and troponin-C) and their isoforms. We show that all the troponin subunits are required for normal myofibril assembly and flight, except for the troponin-C isoform 1 (TnC1). Moreover, rescue experiments conducted with troponin-I embryonic isoform in the IFMs, where flies were rendered flightless, show developmental and functional differences of TnI isoforms and importance of maintaining the right isoform. 

Retracted: No

PubPeer comments:
 ![file] , 
 Thanks to the anonymous reviewer for identifying the mistake in our paper and allowing us to rectify it. Our apology for the unintended mistake. I (S H Singh) habitually make a few good images for the same genotype and used to choose the best one. I believe under the utter rush at the time of paper submission, I jumbled up the images. We will be writing to the journal soon regarding the rectification. We hereby assure that the replacement of the image does not affect or change any of the scientific claims that we have made in our paper. , 
 2019 Correction: https: doi.org 10.1007 s12041-019-1150-x  I believe under the utter rush at the time of paper submission.... this response is a bit strange and will attract more criticism. It is our priority to be responsible. , 
 Corrigendum has been published in the journal. Yes we agree that we should be more careful on organising the figures. ,
Effects of quercetin nanoliposomes on C6 glioma cells through induction of type III programmed cell death
Authors: Gang Wang
Fang Ye
Jun Jie Wang
Rui Ming Li
Jin Bo Feng
Shen Hao Yuan
Ji Yan Chen
Nan Zeng
Shi Ming Du
Guang Yi Yang
Dong Sheng Li
Journal: International Journal of Nanomedicine (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: ATP; C6 glioma cells; liposome; mitochondria; quercetin
Affiliations: Department of Pharmacy, Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, People's Republic of China.

Abstract:  Background: Quercetin has been shown to induce apoptosis in a number of cancer cell lines, but a quercetin-loaded nanoliposomal formulation with enhanced antitumor activity in C6 glioma cells and its effect on cancer cell death has not been well studied. The aim of this study was to examine if quercetin-loaded liposomes (QUE-NL) has enhanced cytotoxic effects and if such effects involve type III programmed cell death in C6 glioma cells. Methods: C6 glioma cells were treated with QUE-NL and assayed for cell survival, apoptosis, and necrosis. Levels of reactive oxygen species production and loss of mitochondrial membrane potential (ΔΨm) were also determined by flow cytometry assay to assess the effects of QUE-NL. ATP levels and lactate dehydrogenase activity were measured, and Western blotting was used to assay cytochrome C release and caspase expression. Results: QUE-NL induced type III (necrotic) programmed cell death in C6 glioma cells in a dose-dependent and time-dependent manner. High concentrations of QUE-NL induced cell necrosis, which is distinct from apoptosis and autophagy, whereas liposomes administered alone induced neither significant apoptosis nor necrosis in C6 glioma cells. QUE-NL-induced ΔΨm loss and cytochrome C release had no effect on caspase activation, but decreased ATP levels and increased lactate dehydrogenase activity indicated that QUE-NL stimulated necrotic cell death. Conclusion: C6 glioma cells treated with QUE-NL showed a cellular pattern associated with necrosis without apoptosis and was independent of caspase activity. Nonapoptotic cell death induced by high concentrations of QUE-NL for controlling caspase-independent type III programmed cell death may provide the basis for novel therapeutic approaches to overcome avoidance of apoptosis by malignant cells. 

Retracted: No

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. ,
Association Between the COVID-19 Pandemic and Infant Neurodevelopment: A Comparison Before and During COVID-19
Authors: Minshan Lu
Yixin Guo
Shanshan Yuan
Huimin Xia
Songying Shen
Antoine Guedeney
Fengjuan Zhou
Jinhua Lu
Xiu Qiu
Peiyuan Huang
Si Tu
Shanshan Lin
Journal: Frontiers in Pediatrics (2021)
Discipline: CLINICAL MEDICINE
Keywords: COVID-19 pandemic; child development; infant behavior; observational study; social isolation.
Affiliations: Division of Birth Cohort Study, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China., Department of Child and Adolescent Psychiatry, Bichat Claude Bernard Hospital, Paris University, Paris, France.

Abstract:  Aim: To investigate the association between the experience of the coronavirus disease 2019 (COVID-19) pandemic and neurodevelopment of 6-month-old and 1-year-old children and explore the differences in the association by birth order. Methods: This comparison study was embedded in the Born in Guangzhou Cohort Study in China. The exposed group included 546 6-month-old and 285 1-year-old children who attended neurodevelopment assessments between March 1 and May 15, 2020, and the non-exposed group included 3,009 6-month-old and 2,214 1-year-old children during the same months from 2015 to 2019. Neurodevelopment at age 6 months and 1 year was assessed by trained clinical staff using the Ages and Stages Questionnaires, third edition (ASQ-3) and the Gesell Developmental Schedules (GDS). Results: The experience of the pandemic in 2020 was associated with a higher risk of delay in the fine motor (adjusted OR: 2.50, 95% CI: 1.25, 4.99; estimated by logistic regression) and communication (adjusted RR [aRR]: 1.13, 95% CI: 1.02, 1.25; estimated by log-binomial regression) domains at age 1 year. The association between the experience of the pandemic and communication delay at age 1 year only existed in first-born children (aRR: 1.15, 95% CI: 1.03, 1.30) but not in later-born children (aRR: 1.02, 95% CI: 0.84, 1.25). No associations were observed in any domain among 6-month-olds. Conclusion: Experiencing the COVID-19 pandemic and related public health strategies might be associated with a higher risk of delay in the development of fine motor and communication in 1-year-old children; the association observed in the communication domain only existed in first-born children. 

Retracted: No

PubPeer comments:
 https: twitter.com tylerblack32 status 1476946267389497383?t=QjlM0jWTyth1wr0qq5LUMw s=09 ,