PReD-Bench/PRed-Bench huggingface dataset:
GZMB gene silencing confers protection against synovial tissue hyperplasia and articular cartilage tissue injury in rheumatoid arthritis through the MAPK signaling pathway
Authors: Xue-Jie Mou
Qi Zhao
Xiang-Kui Zhu
Cui-Xia Bao
Xin-Guang Wang
Hai-Xia Chen
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Articular cartilage tissue injury; GZMB; MAPK signaling pathway; Rheumatoid arthritis; Synovial tissue hyperplasia.
Affiliations: Clinical Laboratory, Yantai Yuhuangding Hospital, Yantai 264000, PR China., Clinical Laboratory, Yeda Hospital, Yantai 264000, PR China., Clinical Laboratory, Yantai Taocun Central Hospital, Yantai 265301, PR China., Department of Radiology, Yantai Oral Hospital, Yantai 264000, PR China., Department of Blood Transfusion, Yeda Hospital, Yantai 264000, PR China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. An Expression of Concern for this article was previously published while an investigation was conducted (see related editorial: https://doi.org/10.1016/j.biopha.2022.113812). This retraction notice supersedes the Expression of Concern published earlier. Concern was raised about the reliability of the Western blot data in Figure 7C, which appear to contain a similar phenotype to those found in other publications, as detailed here: https://pubpeer.com/publications/7DD2DDC979F8CE2B00555332B01F81; and here: https://docs.google.com/spreadsheets/d/1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY/edit#gid=262337249. The journal requested the corresponding author comment on these concerns and provide the associated raw data. The authors did not respond to this request and therefore the Editor-in-Chief decided to retract the article. 

Retracted: No

PubPeer comments:
 I have been curating a collection of manifestations of a pair of Western-Blot proteins blobs. Here, Fig. 4A. and Fig. 7C from [Long et al (2018)] . ![] 5C from [Ao et al (2018)] . ![file] Fig 5 from [Lin et al (2018)] , Fig 9A from [Wu et al (2018)] and 5c from [Wu et al (2018)] . ![] The distinguishing characteristic is a vertical glitch visible at the left end of the left-hand blob in the pair. Anyway, here they are again, in the present Fig 7C:  protein bands examined by Western blot analysis in each group. ![file] ,
Functional INAD complexes are required to mediate degeneration in photoreceptors of the Drosophila rdgA mutant
Authors: Padinjat Raghu
Plamen Georgiev
Isaac Garcia-Murillas
Roger C Hardie
Danny Ulahannan
Journal: Journal of Cell Science (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TRP channels; calcium-influx; phosphoinositide hydrolysis; diacylglycerol; metabolites
Affiliations: The Inositide Laboratory, Babraham Institute, Babraham Research Campus, Cambridge, CB2 4AT, UK, Department of Anatomy, University of Cambridge, Downing St, Cambridge, CB2 3DY, UK

Abstract:  The TRP family of ion channels mediates a wide range of calcium-influx phenomena in eukaryotic cells. Many members of this family are activated downstream of phosphoinositide hydrolysis but the subsequent steps that lead to TRP channel activation in vivo remain unclear. Recently, the lipid products of phosphoinositide hydrolysis (such as diacylglycerol and its metabolites) have been implicated in activating TRP channels in both Drosophila and mammals. In Drosophila photoreceptors, lack of diacylglycerol kinase (DGK) activity (encoded by rdgA) leads to both constitutive TRP-channel activity and retinal degeneration. In this study, using a novel forward-genetic screen, we identified InaD, a multivalent PDZ domain protein as a suppresser of retinal degeneration in rdgA mutants. We show that InaD suppresses rdgA and that the rescue is correlated with reduced levels of phospholipase Cbeta (PLCbeta), a key enzyme for TRP channel activation. Furthermore, we show that light, Gq and PLCbeta all modulate retinal degeneration in rdgA. The results demonstrate a previously unknown requirement for a balance of PLCbeta and DGK activity for retinal degeneration in rdgA. They also suggest a key role for the lipid products of phosphoinositide hydrolysis in the activation of TRP channels in vivo. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] ,
The sensitive detection of single-cell secreted lactic acid for glycolytic inhibitor screening with a microdroplet biosensor
Authors: Yiqiu Zhang
Jun Yan
Xiang Xiao
Zhongyun Jiang
Jian Liu
Sidi Liu
Rui Shen
Xuyue Chen
Baoqing Nie
Journal: Analytical Methods (2020)
Discipline: CHEMISTRY
Keywords: Lactic acid; tumor metabolism; microfluidic approach; droplet biosensors; sensitive detection

Abstract:  Lactic acid (LA) plays an important role in the tumor metabolism and malignant progression of various cancers. Herein, we have developed a one-step, wash-free microfluidic approach with droplet biosensors for the sensitive detection of LA secreted by a single tumor cell. Our assay integrates the enzyme-assisted chemical conversion of LA in small-volume (4.2 nL) droplets for fluorescence signal readout. The microdroplet assay achieved a limit of detection of 1.02 μM and was more sensitive than the commercial ELISA kit by nearly two orders of magnitude. A good specificity has been demonstrated for this assay by testing various ions and biomolecules from the culture medium. This droplet assay allows us to acquire the profiles of the lactic acid secretion of tumor cells under the influence of glycolytic inhibitors at the single-cell level. It offers a useful research tool to study the cell-to-cell differences of LA secretion and glycolytic inhibitor screening for cancer research. 

Retracted: No

PubPeer comments:
 Figure 3 contains 2 panels that seem to appear again as SI data. The images should represent different experiments with different types of cells under different conditions. It is highly unlikely that the same pattern of drops would have occurred by chance. Could the authors check whether they may have inadvertently mixed up the images? ![file] ,
Highly expressed lncRNA LOC730101 promotes lung cancer cell growth through Wnt canonical pathway
Authors: Lei Liu
Yongxue Zhang
Wangkai Cao
Journal: Biochemical and Biophysical Research Communications (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cell proliferation; LOC730101; NSCLC; Wnt/β-catenin.
Affiliations: Department of Oncology, Yantaishan Hospital, China., Department of Thoracic Surgery, Binzhou People's Hospital, China., Department of Thoracic Surgery, The Second People's Hospital of Weifang, China. Electronic address: .

Abstract:  Many long non-coding RNA (lncRNA) has recently been reported to be dysregulated and involved in the progression of non-small-cell lung cancer. However, the biological role of LOC730101 in NSCLC carcinogenesis remains unclear. In the present study, we found that LOC730101 was up-regulated in TCGA and GEO database, so were in NSCLC tissues and cell lines. Overexpression of LOC730101 prompted the proliferation of NSCLC both in vitro and in vivo while Silencing observed opposite phenomenon. Furthermore, we found that LOC730101 enhances the activity of Wnt/β-catenin signaling to promote the progression of cell cycle and ultimate promotes cell proliferation and growth. Therefore, our study may provide a better understanding of the pathogenesis of NSCLC and indicates that LOC730101 may be a potential therapeutic target in NSCLC. 

Retracted: No

PubPeer comments:
 Fig 3D.  Downregulated LOC730101 inhibited ... colony formation (D,E) and leaded cell cycle arrest in G0 G1 stage in H2122 and H522 cell lines . Two of the culture plates appear to be circles cut from a single larger image. ![file] ,
Hyperoxia causes angiopoietin 2–mediated acute lung injury and necrotic cell death
Authors: Michael A Matthay
Jonathan H Nedrelow
Patty J Lee
Antonin R de Fougerolles
Zhou Zhu
Geoffrey L Chupp
Chun G Lee
Vineet Bhandari
Robert J Homer
Lorraine B Ware
Jack A Elias
Rayman Choo-Wing
Xucher Zhang
Anke Geick
Journal: Nature Medicine (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Angiopoietin 2; hyperoxic acute lung injury; vascular leak; endothelial cell apoptosis; oxidant injury
Affiliations: Division of Perinatal Medicine, Yale University School of Medicine, Department of Pediatrics, 333 Cedar Street, New Haven, Connecticut 06520-8064, USA.

Abstract:  The angiogenic growth factor angiopoietin 2 (Ang2) destabilizes blood vessels, enhances vascular leak and induces vascular regression and endothelial cell apoptosis. We considered that Ang2 might be important in hyperoxic acute lung injury (ALI). Here we have characterized the responses in lungs induced by hyperoxia in wild-type and Ang2-/- mice or those given either recombinant Ang2 or short interfering RNA (siRNA) targeted to Ang2. During hyperoxia Ang2 expression is induced in lung epithelial cells, while hyperoxia-induced oxidant injury, cell death, inflammation, permeability alterations and mortality are ameliorated in Ang2-/- and siRNA-treated mice. Hyperoxia induces and activates the extrinsic and mitochondrial cell death pathways and activates initiator and effector caspases through Ang2-dependent pathways in vivo. Ang2 increases inflammation and cell death during hyperoxia in vivo and stimulates epithelial necrosis in hyperoxia in vitro. Ang2 in plasma and alveolar edema fluid is increased in adults with ALI and pulmonary edema. Tracheal Ang2 is also increased in neonates that develop bronchopulmonary dysplasia. Ang2 is thus a mediator of epithelial necrosis with an important role in hyperoxic ALI and pulmonary edema. 

Retracted: No

PubPeer comments:
 Figure 4d. Much more similar than expected. https: imgur.com wVplyWY , 
 In addition to similarities pointed out by Himantolophus Groenlandicus, there could be even more in Fig. 4d: ![file] , 
 #1 Figure 4d continued. Much more similar than expected. https: imgur.com zbD3kZ8 ,
Capsaicin alleviates the imbalance in xenobiotic metabolizing enzymes and tumor markers during experimental lung tumorigenesis
Authors: P Anandakumar
C Naveenkumar
G Ramakrishnan
S Kamaraj
S Asokkumar
S Jagan
T Devaki
Journal: Molecular and Cellular Biochemistry (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Lung cancer; Environmental risk factors; Genotoxic chemicals; Polycyclic aromatic hydrocarbons; Xenobiotic metabolizing enzymes
Affiliations: Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600-025, Tamil Nadu, India.

Abstract:  Lung cancer is currently a leading cause of death all over the world. Environmental risk factors, particularly genotoxic chemicals such as polycyclic aromatic hydrocarbons (PAH), are likely to account for a much higher mortality. Xenobiotic metabolizing enzymes are potentially chief determinants in both the susceptibility to the mutagenic effects of chemical carcinogens and in the response of tumors to chemotherapy. The well-known carcinogen benzo(a)pyrene (B(a)P) of PAH family was given orally (50 mg/kg body weight) to induce lung cancer in Swiss albino mice. B(a)P induction altered the levels of cytochromes (P450, b5), activities of phase I biotransformation enzymes (NADPH-cytochrome P450 reductase, NADH-cytochrome b5 reductase and epoxide hydrolase), phase II enzymes (glutathione-S-transferase, UDP-glucuronyl transferase and DT-diaphorase), and the levels of serum tumor markers. Treatment with capsaicin (CAP) (10 mg/kg body weight) to the lung carcinoma mice restored back the activities of phase I and II biotransformation enzymes and the levels of tumor markers to near normalcy. The above findings were substantiated by immunoblotting and immunohistochemical analysis of cytochrome P450 1A1 (CYP1A1) in the lung tissues. Our present study unravels that CAP can effectively detoxify the carcinogens which discloses its anti-carcinogenic effect during experimental lung cancer. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: Panels a and c appear to show an overlap. Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. ![file] ,
Salvianolic acid B protects SH-SY5Y neuroblastoma cells from 1-methyl-4-phenylpyridinium-induced apoptosis
Authors: Xi Huang
Qing-Hua Liang
Jie-Kun Luo
Yuan Lin
Han-Jun Wu
Guang Zeng
Qi-Dong Yang
Tao Tang
Wan-Hui You
Xing-Qun Li
Journal: Biological & pharmaceutical bulletin (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Parkinson's disease; mitochondrial dysfunction; oxidative stress; apoptotic cascade; salvianolic acid B
Affiliations: Institute of Integrative Medicine, Xiangya Hospital, Central South University, Changsha 410008, P. R. China.

Abstract:  Parkinson's disease (PD) is associated with mitochondrial dysfunction, oxidative stress, and activation of the apoptotic cascade. In the study, we investigated the effects of salvianolic acid B (Sal B) on 1-methyl-4-phenylpyridinium (MPP(+))-treated SH-SY5Y cells, a classic in vitro model for PD. We found Sal B inhibited the loss of cell viability by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The underlying mechanisms of Sal B action were further studied. Treatment of SH-SY5Y cells with MPP(+) caused a loss of cell viability and mitochondrial membrane potential, condensation of nuclei, elevation in the level of reactive oxygen species (which was associated with cytochrome c release), an increase in the Bax/Bcl-2 mRNA ratio, and activation of caspase-3. Sal B ameliorated the MPP(+)-altered phenotypes. These results indicate that the Sal B protected SH-SY5Y cells against MPP(+)-induced apoptosis by relieving oxidative stress and modulating the apoptotic process. Our findings suggest that salvianolic acid B may be a promising agent to prevent PD. 

Retracted: No

PubPeer comments:
 Qi is described as vital energy. Qi is a pseudoscientific, unverified concept, which has never been directly observed, and is unrelated to the concept of energy used in science. How can Journal of Traditional Chinese Medicine be listed as a scientific journal indexed by NLM in PubMed? ,
Sarcoendoplasmic reticulum Ca(2+) ATPase. A critical target in chlorine inhalation-induced cardiotoxicity
Authors: Brian J Day
Shama Ahmad
Aftab Ahmad
Roger L Powell
Tara B Hendry-Hofer
Nichole Reisdorph
Joshua D Chandler
Carl W White
Joan E Loader
Livia A Veress
Christian Schöneich
Olivier Mozziconacci
William C Claycomb
Journal: American Journal of Respiratory Cell and Molecular Biology (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: cardiac; chlorine; inhalation; ranolazine; sarcoendoplasmic reticulum Ca2+ATPase.
Affiliations: 1 Pediatric Airway Research Center, Department of Pediatrics, University of Colorado, Denver, Aurora, Colorado.

Abstract:  Autopsy specimens from human victims or experimental animals that die due to acute chlorine gas exposure present features of cardiovascular pathology. We demonstrate acute chlorine inhalation-induced reduction in heart rate and oxygen saturation in rats. Chlorine inhalation elevated chlorine reactants, such as chlorotyrosine and chloramine, in blood plasma. Using heart tissue and primary cardiomyocytes, we demonstrated that acute high-concentration chlorine exposure in vivo (500 ppm for 30 min) caused decreased total ATP content and loss of sarcoendoplasmic reticulum calcium ATPase (SERCA) activity. Loss of SERCA activity was attributed to chlorination of tyrosine residues and oxidation of an important cysteine residue, cysteine-674, in SERCA, as demonstrated by immunoblots and mass spectrometry. Using cardiomyocytes, we found that chlorine-induced cell death and damage to SERCA could be decreased by thiocyanate, an important biological antioxidant, and by genetic SERCA2 overexpression. We also investigated a U.S. Food and Drug Administration-approved drug, ranolazine, used in treatment of cardiac diseases, and previously shown to stabilize SERCA in animal models of ischemia-reperfusion. Pretreatment with ranolazine or istaroxime, another SERCA activator, prevented chlorine-induced cardiomyocyte death. Further investigation of responsible mechanisms showed that ranolazine- and istaroxime-treated cells preserved mitochondrial membrane potential and ATP after chlorine exposure. Thus, these studies demonstrate a novel critical target for chlorine in the heart and identify potentially useful therapies to mitigate toxicity of acute chlorine exposure. 

Retracted: No

PubPeer comments:
 Figure with duplication ![file] , 
 Thanks for identifying this error. We have now corrected the figure and published the revised version as an erratum in the journal. https: pubmed.ncbi.nlm.nih.gov 33385217 # gid=article-figures pid=figure-4-uid-0 https: pubmed.ncbi.nlm.nih.gov 33385217 ,
DNA damage in mammalian neural stem cells leads to astrocytic differentiation mediated by BMP2 signaling through JAK-STAT
Authors: Silvia K Nicolis
Leonid Schneider
Rebecca Favaro
Federica Pisati
Giuseppe Testa
Serena Pellegatta
Fabrizio d&#x27;Adda di Fagagna
Gaetano Finocchiaro
Paola Roncaglia
Journal: Stem cell reports (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DNA damage; neural stem cells; proliferative arrest; cellular senescence; cytokine secretion
Affiliations: IFOM Foundation-The FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy.

Abstract:  The consequences of DNA damage generation in mammalian somatic stem cells, including neural stem cells (NSCs), are poorly understood despite their potential relevance for tissue homeostasis. Here, we show that, following ionizing radiation-induced DNA damage, NSCs enter irreversible proliferative arrest with features of cellular senescence. This is characterized by increased cytokine secretion, loss of stem cell markers, and astrocytic differentiation. We demonstrate that BMP2 is necessary to induce expression of the astrocyte marker GFAP in irradiated NSCs via a noncanonical signaling pathway engaging JAK-STAT. This is promoted by ATM and antagonized by p53. Using a SOX2-Cre reporter mouse model for cell-lineage tracing, we demonstrate irradiation-induced NSC differentiation in vivo. Furthermore, glioblastoma assays reveal that irradiation therapy affects the tumorigenic potential of cancer stem cells by ablating self-renewal and inducing astroglial differentiation. 

Retracted: No

PubPeer comments:
 It is considered that these papers are duplication. ![file] ![file] ![file] ![file] ![file] ![file] ,
MicroRNA-374 targets JAM-2 regulates the growth and metastasis of human pancreatic cancer cells
Authors: Qi Fang
Zhongchao Zhu
Jian Chang
Jing Tao
Lei Liu
Nan Tang
Wei Li
Journal: American journal of translational research (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Micro-RNA; apoptosis; cell viability; luciferase assay; pancreatic cancer.
Affiliations: Department of Pancreatic Surgery, Renmin Hospital of Wuhan University Wuhan 430060, Hubei, China., Department of Neurosurgery, Union Hospital Tongji Medical College, Huazhong University of Science and Technology Wuhan 430022, Hubei, China.

Abstract:  Pancreatic cancer is one of the devastating human cancers responsible for tremendous human mortality. Current study was undertaken to explore the therapeutic potential of microRNA-374 in human pancreatic cancer. The results showed that microRNA-374 exhibited lower expression in pancreatic cancer cells and tissues. Overexpression of microRNA-374 in cancer cells resulted in significant decrease in the cell viability. The inhibition of the cell viability was mainly due to the induction of apoptosis as evident from the DAPI and AO/EB staining. Annexin V/PI staining also showed that the overexpression of microRNA-374 enhanced the percentage of apoptotic cells. The western blot analysis showed that microRNA-374 overexpression increases Bax and decreased the Bcl-2 expression. The cleaved PARP and Cleaved caspase-3 expression was also considerably increased upon miR-374 overexpression. The TargetScan analysis together with the dual luciferase assay showed that microRNA-374 targets JAM-2 by binding to mRNA at 3'-UTR. The qRT-PCR analysis showed that JAM-2 was significantly upregulated in the pancreatic cancer cell lines and tissues. Moreover, Overexpression of miR-374 suppressed the expression of JAM-2. Additionally, suppression of JAM-2 also inhibited the viability of the pancreatic cancer cells. In vivo studies in xenografted mice models showed that microRNA-374 expression is effective in suppressing the growth and volume of pancreatic tumors. In conclusion, microRNA-374 is downregulated in pancreatic cancers and may exhibit therapeutic implications in the pancreatic cancer treatment. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have partially overlapping images ![file] , 
 Fig 4A. ![file] ,
Increase of autophagy and attenuation of apoptosis by Salvigenin promote survival of SH-SY5Y cells following treatment with H₂O₂
Authors: Fariba Khodagholi
Mahdi Moridi Farimani
Shahnaz Babaei Abraki
Ghazaleh Rafatian
Mossa Gardaneh
Journal: Molecular and Cellular Biochemistry (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Oxidative stress; Salvigenin; neuroprotective effect; apoptosis; autophagy
Affiliations: Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Abstract:  Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. Here, we tried to elucidate the possible neuroprotective effect of Salvigenin, a natural polyphenolic compound, on oxidative stress-induced apoptosis and autophagy in human neuroblastoma SH-SY5Y cells. We measured cell viability by MTT test and found that 25 μM is the best protective concentration of Salvigenin. GSH and SOD assays suggested that Salvigenin activates antioxidant factors. At the same time, measurement of ER stress-associated proteins including calpain and caspase-12 showed the ability of Salvigenin to decrease ER stress. We found that Salvigenin could decrease the apoptotic factors. Salvigenin inhibited H(2)O(2)-induced caspase-3 which is a hallmark of apoptosis in addition to reducing Bax\Bcl-2 ratio by 1.45 fold. Additionally, Salvigenin increased the levels of autophagic factors. Our results showed an increase in LC3-II/LC3-I ratio, Atg7, and Atg12 in the presence of 25 μM of Salvigenin by about 1.28, 1.25, and 1.54 folds, respectively, compared to H(2)O(2)-treated cells. So it seems that H(2)O(2) cytotoxicity mainly results from apoptosis. Besides, Salvigenin helps cells to survive by inhibiting apoptosis and enhancing autophagy that opens a new horizon for the future experiments. 

Retracted: No

PubPeer comments:
 Figure 5D: An area visible in the mAb AA98 photo appears to also be visible in the Vorinostat+mIgG photo. Highlighted in red. ![file] , 
 In Figure 5E, a very similar looking brown stain is visible in both the mAb AA98 as well as the Vorinostat+mIgG photos. Highlighted in purple. ![file] , 
 Expression of Concern, [March 2020] :  The editors are publishing this note to alert readers to a concern about this article (1). In Fig. 5D, similarities exist in the mAb AA98 and Vorinostat + mIgG slides. The authors stand by the conclusions in the article. For some reason this is billed on the main page as a  Correction , although nothing is corrected. ![file] , 
 Not explicitly mentioned in the EoC, there seems to be a duplicated region *within* an image in Figure 5E, although the circled areas do not seem identical. *** ![file] *** Grant support: National Science Foundation of China (nos. 30700895, 30770913, 30770914, 30801224, and 30528012), NCET-04-0719, and u201c973u201d Program (2009CB521800). ,
miR-29a/b enhances cell migration and invasion in nasopharyngeal carcinoma progression by regulating SPARC and COL3A1 gene expression
Authors: Tianyu Guo
Songmei Zhang
Xuejun Wang
Ying Yu
Bingcheng Zou
Jun Xie
Feifei Qiu
Qing Zhang
Ning Deng
Yange Cao
Tao Ling
Rui Sun
Tao Jing
Journal: PLoS ONE (2015)
Discipline: Multidisciplinary
Keywords: Nasopharyngeal carcinoma; miRNAs; migration; invasion; genes
Affiliations: State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China., State Key Laboratory of Oncology in Southern China; Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China., Key Laboratory of Molecular Immunology and Antibody Engineering of Guangdong Province, Antibody Engineering Center in Jinan University, Guangzhou, China., Key Laboratory of Tropical & Subtropical Fishery Resource Application & Cultivation, Ministry of Agriculture, Pearl River Fisheries Research Institute of CAFS, Guangzhou, Guangdong, China.

Abstract:  Nasopharyngeal carcinoma (NPC) is a malignant tumor associated with a genetic predisposition, Epstein-Barr virus infection and chromosomal abnormalities. Recently, several miRNAs have been shown to target specific mRNAs to regulate NPC development and progression. However, the involvement of miRNAs in processes leading to NPC migration and invasion remains to be elucidated. We predicted that miR-29a/b are associated with dysregulated genes controlling NPC through an integrated interaction network of miRNAs and genes. miR-29a/b over-expression in NPC cell lines had no significant effect on proliferation, whereas miR-29b mildly increased the percentage of cells in the G1 phase with a concomitant decrease in the percentage of cells in S phase. Furthermore, we demonstrated that miR-29a/b might be responsible for increasing S18 cell migration and invasion, and only COL3A1 was identified as a direct target of miR-29b despite the fact that both SPARC and COL3A1 were inhibited by miR-29a/b over-expression. Meanwhile, SPARC proteins were increased in metastatic NPC tissue and are involved in NPC progression. Unexpectedly, we identified that miRNA-29b expression was elevated in the serum of NPC patients with a high risk of metastasis. The 5-year actuarial overall survival rates in NPC patients with high serum miR-29b expression was significantly shorter than those with low serum miR-29b expression; therefore, serum miR-29b expression could be a promising prognostic marker. 

Retracted: No

PubPeer comments:
 Fig. 5B and Fig. 5C. The WB bands shown in different color boxes appear more similar than expected. ![file] , 
 Further, one band appears spliced after contrast enhancement: ![file] ,
Comparative Analysis Identifies Exonic Splicing Regulatory Sequences—The Complex Definition of Enhancers and Silencers
Authors: Gil Ast
Galit Lev-Maor
Tal Pupko
Hadas Keren
Ida Vig
Maayan Amit
Oren Ram
Amir Goren
Journal: Molecular Cell (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Exonic splicing regulatory sequences; ESRs; alternative splicing; conservation level; wobble positions
Affiliations: Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.

Abstract:  Exonic splicing regulatory sequences (ESRs) are cis-acting factor binding sites that regulate constitutive and alternative splicing. A computational method based on the conservation level of wobble positions and the overabundance of sequence motifs between 46,103 human and mouse orthologous exons was developed, identifying 285 putative ESRs. Alternatively spliced exons that are either short in length or contain weak splice sites show the highest conservation level of those ESRs, especially toward the edges of exons. ESRs that are abundant in those subgroups show a different distribution between constitutively and alternatively spliced exons. Representatives of these ESRs and two SR protein binding sites were shown, experimentally, to display variable regulatory effects on alternative splicing, depending on their relative locations in the exon. This finding signifies the delicate positional effect of ESRs on alternative splicing regulation. 

Retracted: No

PubPeer comments:
 Fig. 4c u2013 more similar than expected. Could authors check please? ![file] , 
 #1 I concur with the concerns about Fig 4c. Fortunately, the journal figures are mostly quite good quality (go to the  high-res versions at the HTML page). Unfortunately, there are many other figures with similarly concerning irregularities, including apparent duplications and unusual background smudges, boxes, etc. See examples below. I may have missed some. Images were enhanced by adjusting gradient maps in Photoshop. (Click images to enlarge.) * Fig 3B-3C: ![file] * Fig 3E: ![file] * Fig 5B-5C *(some lanes are much lower resolution, obscuring the degree of similarity)*: ![file] * Fig 5E: ![file] * Fig 5G: ![file] , 
 #1 #2 Excellent figure sleuthing from the combined actions of these two Central American hawkmoths. Much of the lane and band splicing is visible in a Fiji Spectrum LUT of Fig. 4C. The first 3 lanes come from a different source. The ragged top splice edges in lanes 4-9 are a bit of a giveaway. *Manduca* might be hoping to see original data, but is undoubtedly going to be disappointed. ![image] , 
 #2 An addendum: in addition to the apparent duplications that were previously noted ***within*** Figure panels, there appears to be some sharing ***between*** Figure panels 3E and 5G, as annotated below. (Note, the Fig 3E lanes appear to be vertically compressed relative to those in Fig 5G.) ![file] ,
Bio-isosteric replacement of amide group with 1,2,3-triazole in phenacetin improves the toxicology and efficacy of phenacetin-triazole conjugates (PhTCs)
Authors: Debashree Das
Adarsh Sahu
Ram Kishore Agrawal
Asmita Gajbhiye
Journal: Life Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 1,2,3-triazole; Amide bond; Analgesic; Anti-inflammatory; Anti-pyretic
Affiliations: Department of Pharmaceutical Sciences, Dr. Harisingh Gour Central University, Sagar, MP, India. Electronic address: ., Department of Pharmaceutical Sciences, Dr. Harisingh Gour Central University, Sagar, MP, India.

Abstract:  Aim: Inflammatory algesia and pyresia are common pathological consequences of physiological defense. Phenacetin introduced as effective analgesic anti-pyretic agent, was proscribed from therapeutic use because of associated systemic toxicity. The aim of the study was to evaluate the potency of 1,2,3-triazole conjugation in reducing toxicity and increasing efficacy of the phenacetin nucleus. Main methods: The amide bond implicated as the cause of phenacetin toxicity was bioisosterically replaced with 1,2,3-triazoles to yield a series of PhTCs(PhTC1, PhTC2 and PhTC3). The toxicology of the synthesized conjugates in reference to phenacetin was evaluated in accordance with OECD test guidelines 420, 425 and 407. For the purpose of evaluating anti-inflammatory potency carrageenan induced paw edema and croton oil induced ear edema models were evaluated. Anti-nociceptive efficacy was assessed using Eddy's hot plate and acetic acid induced writhing experimental models. For anti-pyretic efficacy, the conjugates were submitted to Brewer's yeast antipyretic assay. Key findings: Toxicological examination of PhTCs in comparison to phenacetin revealed that, phenacetin treatment caused considerable nephrotoxicity and hepatotoxicity in experimental models PhTCs were devoid of such toxic manifestations. Results of pharmacological assays showed that the entire series of PhTCs possessed better anti-inflammatory, anti-nociceptive and anti-pyretic potential than phenacetin. Furthermore it was revealed that the pharmacological profile of PhTC1 with triazole substitution at para position of the phenol ring exhibited potency even better than that exhibited by the reference standards. Conclusion: Bioisosteric replacement of amide bond by 1,2,3-triazole in the phenacetin moiety yields conjugates with superior efficacy and diminished toxicity, thus opening neo avenues in treatment of inflammatory syndromes. 

Retracted: No

PubPeer comments:
 More similar than one would expect in Fig 1. ![file] Suspected image duplication in Fig 4. ![file] ,
Chemosensitization by a non-apoptogenic heat shock protein 70-binding apoptosis-inducing factor mutant
Authors: Arnaud Parcellier
Sandeep Gurbuxani
Maria Celia Morales
Elise Schmitt
Marja Jäättelä
Fabrizio Giordanetto
Clayton R Hunt
David J Dix
Arlette Hammann
Josef M Penninger
Carmen Garrido
Celine Cande
Alena Pance
Guido Kroemer
Romano T Kroemer
Journal: Cancer Research (2003)
Discipline: CLINICAL MEDICINE
Keywords: Heat shock protein 70; apoptosis; tumorigenicity; cancer cells; caspase activator
Affiliations: Institut National de la Santé et de la Recherché Médicale U-517, Faculty of Medicine and Pharmacy, Dijon, France.

Abstract:  Heat shock protein 70 (HSP70) inhibits apoptosis and thereby increases the survival of cells exposed to a wide range of lethal stimuli. HSP70 has also been shown to increase the tumorigenicity of cancer cells in rodent models. The protective function of this chaperone involves interaction and neutralization of the caspase activator apoptotic protease activation factor-1 and the mitochondrial flavoprotein apoptosis-inducing factor (AIF). In this work, we determined by deletional mutagenesis that a domain of AIF comprised between amino acids 150 and 228 is engaged in a molecular interaction with the substrate-binding domain of HSP70. Computer calculations favored this conclusion. On the basis of this information, we constructed an AIF-derived protein, which is cytosolic, noncytotoxic, yet maintains its capacity to interact with HSP70. This protein, designated ADD70, sensitized different human cancer cells to apoptosis induced by a variety of death stimuli by its capacity to interact with HSP70 and therefore to sequester HSP70. Thus, its chemosensitizing effect was lost in cells in which inducible HSP70 genes had been deleted. These data delineate a novel strategy for the selective neutralization of HSP70. 

Retracted: No

PubPeer comments:
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 #1 When this paper was published there were no clear rules of how a Figure should be assembled. There is no splicing in the HSP70 panel because for that Ab the samples (in the desired position) were run in another gel. Carmen Garrido , 
 #2 When this paper was published there were no rules of how a Figure should be assembled. There is no splicing in the HSP70 panel because for that Ab the samples (in the desired position) were run in another gel. Carmen Garrido , 
 #3 Comment 3: Same bands for AIF in D567-609 (Fig. 1B, 2nd lane) and R192 (Fig. 1E, 4th lane) After retrieving the corresponding bands and zooming them, it is clear that although there is a resemblance between the bands, they are clearly not identical, neither in the contour nor in the contrast. Moreover, the background appears different. Note the different positions of faint signals on the right side of both bands. Carmen Garrido , 
 #6 Could the authors illustrate that? ,
Centella asiatica prevents D-galactose-Induced cognitive deficits, oxidative stress and neurodegeneration in the adult rat brain
Authors: Neha Singh
Zeba Firdaus
Santosh Kumar Prajapati
Sairam Krishnamurthy
Tryambak Deo Singh
Journal: Drug and Chemical Toxicology (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Acetylcholinesterase; Centella asiatica; D-galactose; Gotu kola; cognitive impairment
Affiliations: Department of Medicinal Chemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India., Department of Pathology, MSR Medical College, Bengaluru, India., Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology, BHU, Varanasi, India.

Abstract:  Chronic D-galactose (D-gal) administration causes cognitive impairment and is used widely in animal models for anti-aging studies. Centella asiatica (CA), a traditional herbal medicine, has been used as a brain tonic to enhance memory. This study evaluates the neuroprotective role of an ethanolic extract of Centella asiatica (CAE) against D-gal-induced aging in rats. Healthy male rats were divided into three groups: Control, D-gal, and D-gal + CAE. The Control group received normal saline (i.p.), whereas the D-gal group received D-gal (120 mg/kg b.w., i.p.), and the D-gal + CAE group received D-gal (120 mg/kg b.w., i.p.) and CAE (300 mg/kg b.w., orally) daily for 42 days. Behavioral and brain biochemical and histopathological changes were assessed after treatment. The results of the behavioral study depicted that D-gal significantly reduces the spontaneous alternation and locomotor activity indicating behavioral and cognitive impairment. Biochemical studies showed that D-gal significantly increases the oxidative stress and acetylcholinesterase activity (AChE) in rat brain. Histopathological study showed that D-gal disturbs the normal architecture of hippocampal and cortical cells, indicating degeneration in these brain areas. D-gal and CAE co-treatment for 42 days attenuated the behavioral, biochemical, and neuroanatomical impairments caused by the D-gal; it markedly suppresses the D-gal-induced oxidative stress and AChE activity in the brain, and maintains the normal cellular architecture in hippocampal and cortical areas. Thus, this study shows that CAE can protect the brain from the adverse effects of D-gal (e.g., memory loss and cognitive impairment) by modulating AChE activity and oxidative stress. 

Retracted: No

PubPeer comments:
 The paper represents the similar Animal Ethical Committee Number (542 02 ab CPCSEA, 27.12.2012) Which is already mentioned in the previous article (Pandey S. In vitro drug release and study of anti-inflammatory effect of Rasna Saptak Kwath. Asian Journal of Pharmacotics, 2018 Feb 7; 11 (04). While any author of the last published article (Pandey et al., 2018), have not contributed to this article. ,
Therapeutical effects and mechanism of salubrinal combined with ulinastatin on treating paraquat poisoning
Authors: Xiaomin Sun
Chao Jiang
Hua Guo
Journal: Cell Biochemistry and Biophysics (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Therapeutic effects; Salubrinal; Ulinastatin; Acute Paraquat poisoning; Lung tissue
Affiliations: Department of Emergency, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China, .

Abstract:  To explore therapeutic effects and underlying mechanism of Salubrinal combined with Ulinastatin (UTI) on acute Paraquat (PQ) poisoning. Four hundred rats were randomly allocated into UTI group, SAL group, SAL + UTI and control group according to random number table with 100 rats in each group. Acute PQ poisoning models were established, and all rats received UTI, Salubrinal, SAL + UTI and normal saline injection, respectively. Afterward, we analyzed the change of lung tissue and explored the mechanism. Acute PQ poisoning caused significantly damage in rat lung tissue structure, and UTI could effectively repair lung tissue damage. Salubrinal suppressed hemorrhage and fibrosis, but promoted inflammatory infiltration. In contrast, UTI + Salubrinal suppressed hemorrhage, fibrosis and inflammatory infiltration, but could not improve lung tissue damage. Expression of LC3 and Bcl-2 showed statistically significant difference among different groups (p &lt; 0.05). LC3 and Bcl-2 levels in UTI group were much higher than in the other groups, and LC3 and Bcl-2 levels in UTI + SAL group was second higher. LC expression in SAL group was lower than in UTI group and UTI + SAL group with Bcl-2 in control group significantly lower than in the other groups (p &lt; 0.05). Expression of Caspase-3 and Bcl-2/Bax in lung tissue in different groups had statistically significant difference (p &lt; 0.05). Caspase-3 in UTI group was lower than in the other groups; however, Bcl-2/Bax in UTI group was higher than in the other groups (p &lt; 0.05). Acute PQ poisoning can cause endoplasmic reticulum stress-autophagy in rat, and UTI can increase Bcl-2 expression, decrease Caspase-3, which can inhibit progress of lung injury by suppressing apoptosis and exert good therapeutic effects. Although salubrinal has marked effects on protecting lung tissue, it can increase Bcl-2 expression, which is not beneficial to lung tissue protection. The underlying mechanism still needs further exploration. 

Retracted: No

PubPeer comments:
 1. Figs 2, 3, and 5 are using the same beta-actin 2. Figs 3 and 5 basically are the same figure Can the authors explain? ![file] ,
MicroRNA-98 Attenuates Cell Migration and Invasion in Glioma by Directly Targeting Pre-B Cell Leukemia Homeobox 3
Authors: Yinlong Liu
Xiupeng Xu
Zhongyuan Bao
Ning Liu
Jing Ji
Journal: Cellular and Molecular Neurobiology (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Glioma; Invasion; Migration; PBX3; miR-98.
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China., Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China. .

Abstract:  Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. The extraordinary invasion of human GBM into adjacent normal brain tissues contributes to treatment failure. However, the mechanisms that control this process remain poorly understood. Increasing evidence has demonstrated that microRNAs are strongly implicated in the migration and invasion of GBM. In this study, we found that microRNA-98 (miR-98) was markedly downregulated in human glioma tissues and cell lines. Functional experiments indicated that restored expression of miR-98 attenuated glioma cell invasion and migration, whereas depletion of miR-98 promoted glioma cell invasion and migration. Subsequent investigation showed that pre-B-cell leukemia homeobox 3 (PBX3), an important transcription factor that controls tumor invasion, was a direct and functional target of miR-98 in GBM cells. Consistently, an orthotopic mouse model also demonstrated the suppressive effects of miR-98 overexpression on tumor invasion and PBX3 expression. Silencing of PBX3 using small interfering RNA inhibited the migratory and invasive capacities of glioma cells, whereas reintroduction of PBX3 into glioma cells reversed the anti-invasive function of miR-98. Furthermore, depletion of PBX3 phenocopied the effects of miR-98 overexpression in vivo. Finally, quantitative real-time polymerase chain reaction results showed that miR-98 was negatively correlated with PBX3 expression in 24 glioma tissues. Thus, we propose that PBX3 modulation by miR-98 has an important role in regulating GBM invasion and may serve as therapeutic target for GBM. 

Retracted: No

PubPeer comments:
 There appears to be several image duplications in figures 2, 4, and 5 (with the coloring different). ![file] Figure 4 again: ![file] ,
Long non-coding RNA Unigene56159 promotes epithelial–mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells
Authors: Jing-Yi Fan
Xiao-Pei Zhao
Min Liu
Yi Zhang
Jing Lv
Ping Lv
Hong-Xia Fan
Hua Tang
Journal: Cancer Letters (2016)
Discipline: CLINICAL MEDICINE
Keywords: HCC migration/invasion; Long non-coding RNA (lncRNA); Slug; lncRNA-Unigene56159; miR-140-5p.
Affiliations: Tianjin Life Science Research Center and Department of Pathology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China., Tianjin Life Science Research Center and Department of Pathology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China. Electronic address: .

Abstract:  HBV infection has been reported to be closely associated with HCC development; however, the underlying mechanisms are unclear. Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play important regulatory roles in the pathogenesis and progression of cancers. To investigate the important role and mechanism of lncRNAs in the progression of HBV-related HCC, we screened lncRNAs in HBV-positive and HBV-negative HCC tissues. We identified a novel lncRNA, lncRNA-Unigene56159, which is highly expressed in HBV-related HCC tissues, and further analysis showed that this lncRNA was induced by HBV in vitro. Functionally, Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug. Collectively, our findings indicate that the Unigene56159/miR-140-5p/Slug axis contributes to HCC cell migration and invasion, which may provide novel insights into the function of lncRNA-driven hepatocarcinogenesis. 

Retracted: No

PubPeer comments:
 The authors regret In the original version of the article, the transwell migration and invasion images for pshR1 + 3-Unigene 56159 groups in Fig. 2D were placed by mistake. The corrected version of Fig. 2 was provided below. This correction does not change the results or conclusions of this paper. I apologise for this mistake due to our carelessness. The authors would like to apologise for any inconvenience caused. ![file] , 
 Could the authors also please take a look at Figure 5E? There appears to be an overlap between two panels that represent different experiments. I have marked the possible overlap here with red boxes. ![file] ,
Induction of human bone marrow mesenchymal stem cells differentiation into neural-like cells using cerebrospinal fluid
Authors: Xian-Fu Lu
Yin-Ming Zeng
Ying Ye
Mei-Rong Wan
Journal: Cell Biochemistry and Biophysics (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: bone marrow mesenchymal stem cells; neural-like cells; cerebrospinal fluid; induction technique; differentiation
Affiliations: Department of Anesthesiology, the first Affiliated Hospital, China Medical University, Shenyang, 110001, China. 

Abstract:  To optimize a technique that induces bone marrow mesenchymal stem cells (BMSCs) to differentiation into neural-like cells, using cerebrospinal fluid (CSF) from the patient. In vitro, CSF (Group A) and the cell growth factors EGF and bFGF (Group B) were used to induce BMSCs to differentiate into neural-like cells. Post-induction, presence of neural-like cells was confirmed through the use of light and immunofluorescence microscopy. BMSCs can be induced to differentiate into neural-like cells. The presence of neural-like cells was confirmed via morphological characteristics, phenotype, and biological properties. Induction using CSF can shorten the production time of neural-like cells and the quantity is significantly higher than that obtained by induction with growth factor (P &lt; 0.01). The two induction methods can induce BMSCs to differentiate into neural-like cells. Using CSF induction, 30 ml bone marrow can produce a sufficient number of neural-like cells that totally meet the requirements for clinical treatment. 

Retracted: No

PubPeer comments:
 Figures 3A and 3B appear to overlap. *** ![file] ,