PReD-Bench/PRed-Bench huggingface dataset:
RETRACTED ARTICLE: Construction of pancreatic cancer double-factor regulatory network based on chip data on the transcriptional level
Authors: Li-Li Zhao
Li-Wei Zhuang
Na Tao
Bing-Rong Liu
Tie-Fu Liu
Tong Zhang
Journal: Molecular Biology Reports (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Transcription factor; microRNA; pancreatic cancer; DEGs; KEGG pathway
Affiliations: Department of Gastroenterology, The Fourth Affiliated Hospital of Harbin Medical University, No. 37 Yiyuan Street, Nangang District, Harbin, 150001, Heilongjiang, China.

Abstract:  Transcription factor (TF) and microRNA (miRNA) have been discovered playing crucial roles in cancer development. However, the effect of TFs and miRNAs in pancreatic cancer pathogenesis remains vague. We attempted to reveal the possible mechanism of pancreatic cancer based on transcription level. Using GSE16515 datasets downloaded from gene expression omnibus database, we first identified the differentially expressed genes (DEGs) in pancreatic cancer by the limma package in R. Then the DEGs were mapped into DAVID to conduct the kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis. TFs and miRNAs that DEGs significantly enriched were identified by Fisher's test, and then the pancreatic cancer double-factor regulatory network was constructed. In our study, total 1117 DEGs were identified and they significantly enriched in 4 KEGG pathways. A double-factor regulatory network was established, including 29 DEGs, 24 TFs, 25 miRNAs. In the network, LAMC2, BRIP1 and miR155 were identified which may be involved in pancreatic cancer development. In conclusion, the double-factor regulatory network was found to play an important role in pancreatic cancer progression and our results shed new light on the molecular mechanism of pancreatic cancer. 

Retracted: Yes

PubPeer comments:
 This article was retracted on 18 August 2015 The Publisher and Editor retract this article in accordance with the recommendations of the Committee on Publication Ethics (COPE). After a thorough investigation we have strong reason to believe that the peer review process was compromised. ,
Oroxylin A inhibits invasion and migration through suppressing ERK/GSK-3β signaling in snail-expressing non-small-cell lung cancer cells
Authors: Li Zhao
Kai Zhao
Qinglong Guo
Yuxin Zhou
Yujie Huang
Libin Wei
Yuyuan Yao
Na Lu
Journal: Molecular carcinogenesis (2016)
Discipline: CLINICAL MEDICINE
Keywords: E-cadherin; ERK; GSK-3β; oroxylin A; snail.
Affiliations: State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of Education, Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing, P.R. China.

Abstract:  Snail is closely linked to tumor invasion, metastasis, and recurrence and indicates prognosis of patients suffering from cancer. Overexpression of Snail increases motility and invasiveness of cancer cells, which has become target for anti-metastatic treatment. Oroxylin A, a natural compound extracted from Scutellaria radix, has been reported to inhibit invasion and migration in breast cancer. In this study, we investigated the anti-invasive effect of oroxylin A on lung cells and uncovered its underlying mechanism. The results suggested that oroxylin A could inhibit migration and invasion in Snail-expressing 95-D, and A549 cells whereas it had little effect on non-expressing GLC-82 cells. Furthermore, enhanced Snail expression after transfection of Snail vector in GLC-82 cells is decreased by oroxylin A. Snail can also induce epithelial-mesenchymal transition. We found oroxylin A could reverse TGFβ1-induced epithelial-mesenchymal transition by inhibiting Snail expression. As a result, oroxylin A up-regulated E-cadherin expression and down-regulated vimentin, MMP-9, and CD44v6 expression, which could lead to the inhibition of tumor migration and invasion. Mechanically, we demonstrated that oroxylin A suppressed activation of ERK instead of AKT pathway and then promoted activation of GSK-3β to reduce Snail protein content. Finally, we established transplanted, metastatic, and orthotopic models of A549 cells, and found that oroxylin A inhibited the growth and lung metastasis of A549 cells in vivo. Taken together, we proposed that oroxylin A might be a promising candidate targeting tumor metastasis. © 2016 Wiley Periodicals, Inc. 

Retracted: No

PubPeer comments:
 This article appears to be computer-generated with [SCIgen] . ![file] --- This comment was written by Guillaume Cabanac and Cyril Labbu00e9. Contact: [SeekAndBlastn-Operators@univ-grenoble-alpes.fr](mailto:SeekAndBlastn-Operators@univ-grenoble-alpes.fr). ,
Four glial cells regulate ER stress resistance and longevity via neuropeptide signaling in C. elegans
Authors: Raz Bar-Ziv
Melissa G Metcalf
Andrew Dillin
Nazineen Kandahari
Ashley E Frakes
Sarah U Tronnes
Jenni Durieux
Holly K Gildea
Samira Monshietehadi
Journal: Science (2020)
Discipline: Multidisciplinary
Keywords: nervous system; cellular stress; protein homeostasis; organismal health; stress responses
Affiliations: Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA., Howard Hughes Medical Institute, University of California, Berkeley, CA 94720, USA., Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. .

Abstract:  The ability of the nervous system to sense cellular stress and coordinate protein homeostasis is essential for organismal health. Unfortunately, stress responses that mitigate disturbances in proteostasis, such as the unfolded protein response of the endoplasmic reticulum (UPRER), become defunct with age. In this work, we expressed the constitutively active UPRER transcription factor, XBP-1s, in a subset of astrocyte-like glia, which extended the life span in Caenorhabditis elegans Glial XBP-1s initiated a robust cell nonautonomous activation of the UPRER in distal cells and rendered animals more resistant to protein aggregation and chronic ER stress. Mutants deficient in neuropeptide processing and secretion suppressed glial cell nonautonomous induction of the UPRER and life-span extension. Thus, astrocyte-like glial cells play a role in regulating organismal ER stress resistance and longevity. 

Retracted: No

PubPeer comments:
 This paper is very much rushed and seems to have many holes. Just to name a few: 1. Fig. 2A and B shows the results from worms fed with RNAi Ecoli. Worm RNAi feeding is known to be not effective in the nervous system. The authors can test it using mutant worms rather than RNAi feeding. In case they want to use RNAi, they need to show the decrease of gene levels using qPCR or western blot. 2. The authors concluded from Fig. 3A that  (the treatment) reduced aggregation of ......polyQ protein...... . I think the conclusion should be the treatment reduced the expression level of polyQ protein. Because I do not see the change of polyQ protein from evenly distributed to aggregation. 4. The authors claim there is a moderate increase in GFP signal in Fig. S12D. There is no quantification of signal intensity. And in my eyes, there is no increase in signal, not even a moderate one. ,
Nuclear factor-kappaB p65 facilitates longitudinal bone growth by inducing growth plate chondrocyte proliferation and differentiation and by preventing apoptosis
Authors: Janna K Flint
Shufang Wu
Geoffrey Rezvani
Francesco De Luca
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: NF-kappaB; bone growth; chondrocytes; proliferation; differentiation
Affiliations: Section of Endocrinology and Diabetes, St. Christopher's Hospital for Children, Department of Pediatrics, Drexel University College of Medicine, Philadelphia, Pennsylvania 19134, USA.

Abstract:  NF-kappaB is a group of transcription factors involved in cell proliferation, differentiation, and apoptosis. Mice deficient in the NF-kappaB subunits p50 and p52 have retarded growth, suggesting that NF-kappaB is involved in bone growth. Yet, it is not clear whether the reduced bone growth of these mice depends on the lack of NF-kappaB activity in growth plate chondrocytes. Using cultured rat metatarsal bones and isolated growth plate chondrocytes, we studied the effects of two NF-kappaB inhibitors (pyrrolidine dithiocarbamate (PDTC) or BAY11-7082 (BAY)), p65 short interference RNA (siRNA), and of the overexpression of p65 on chondrocyte proliferation, differentiation, and apoptosis. To further define the underlying mechanisms, we studied the functional interaction between NF-kappaB p65 and BMP-2 in chondrocytes. PDTC and BAY suppressed metatarsal linear growth. Such growth inhibition resulted from decreased chondrocyte proliferation and differentiation and from increased chondrocyte apoptosis. In cultured chondrocytes, the inhibition of NF-kappaB p65 activation (by PDTC and BAY) and expression (by p65 siRNA) led to the same findings observed in cultured metatarsal bones. In contrast, overexpression of p65 in cultured chondrocytes induced chondrocyte proliferation and differentiation and prevented apoptosis. Although PDTC, BAY, and p65 siRNA reduced the expression of BMP-2 in cultured growth plate chondrocytes, the overexpression of p65 increased it. The addition of Noggin, a BMP-2 antagonist, neutralized the stimulatory effects of p65 on chondrocyte proliferation and differentiation, as well as its anti-apoptotic effect. In conclusion, our findings indicate that NF-kappaB p65 expressed in growth plate chondrocytes facilitates growth plate chondrogenesis and longitudinal bone growth by inducing BMP-2 expression and activity. 

Retracted: Yes

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
RETRACTED ARTICLE: Global analysis of streamflow response to forest management
Authors: Jaivime Evaristo
Jeffrey J McDonnell
Journal: Nature (2019)
Discipline: Multidisciplinary
Keywords: Streamflow response; Forest management; Water yield; Vegetation-to-bedrock model; Landscape factors
Affiliations: Copernicus Institute of Sustainable Development, Utrecht University, Utrecht, The Netherlands. ., Global Institute for Water Security, School of Environment and Sustainability, University of Saskatchewan, Saskatoon, Canada., School of Resources and Environmental Engineering, Ludong University, Yantai, China., School of Geography, Earth and Environmental Sciences, University of Birmingham, Birmingham, UK.

Abstract:  Predicting the responses of streamflow to changes in forest management is fundamental to the sustainable regulation of water resources. However, studies of changes in forest cover have yielded unclear and largely unpredictable results. Here we compile a comprehensive and spatially distributed database of forest-management studies worldwide, to assess the factors that control streamflow response to forest planting and removal. We introduce a vegetation-to-bedrock model that includes seven key landscape factors in order to explain the impacts of forest removal and planting on water yield. We show that the amount of water stored in a landscape is the most important factor in predicting streamflow response to forest removal, whereas the loss of water through evaporation and transpiration is the most important factor in predicting streamflow response to forest planting. Our findings affect model parameterizations in climate change mitigation schemes (involving, for example, afforestation or deforestation) in different geologic and climate regions around the world, and inform practices for the sustainable management of water resources. 

Retracted: No

PubPeer comments:
 See https: retractionwatch.com 2020 02 18 authors-retract-nature-paper-on-dramatic-increases-in-streamflow-from-deforestation for backgrounds. ,
miRNAs in vascular integrity
Authors: Pei-Ying Zhang
Yong Cao
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: cardiovascular diseases; endothelial cell regulation; miRNAs.
Affiliations: Department of Cardiology, Xuzhou Hospital of Traditional Chinese Medicine, Xuzhou, Jiangsu 221009, P.R. China., Department of Cardiology, Xuzhou Central Hospital, The Affiliated Xuzhou Hospital of Medical College of Southeast University, Xuzhou, Jiangsu 221009, P.R. China.

Abstract:  Endothelial cells (ECs) are confirmed as important regulators of vascular integrity, particularly in relation to angiogenesis, wound repair post-injury, and during embryogenesis. Futher, miRNAs have been implicated in EC function and proliferation. Moreover, knockdown of these miRNAs resulted in altered expressions of several important regulators of endothelial biology and angiogenesis including vascular endothelial growth factor receptor 2, endothelial nitric oxide synthase and tubule formation capacity. Several miRNAs have been identified to play a role in the regulation of function, proliferation and growth of vascular ECs. These miRNAs may be important therapeutic targets in the treatment of a range of ischemic diseases, as well as in the regulation of angiogenesis during cancer and tumour progression. The present review discuss some of the important miRNAs having confirmed regulatory role in EC in connection espically with cardiovascular disease. 

Retracted: No

PubPeer comments:
 This paper owes an unacknowledged debt to  MicroRNA regulation of endothelial homeostasis and commitmentu2014implications for vascular regeneration strategies using stem cell therapies [(Scott et al 2013)] . This is most obvious when comparing the present Fig 1... ![file] ...with Fig 1 from Scott et al. ![] ,
MiR-429 inhibits cells growth and invasion and regulates EMT-related marker genes by targeting Onecut2 in colorectal carcinoma
Authors: Yingnan Sun
Zeyou Wang
Xiaoping Liu
Shourong Shen
Minghua Wu
Hailin Tang
Xiayu Li
Zhibin Yu
Journal: Molecular and Cellular Biochemistry (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: colorectal cancer; epithelial-mesenchymal transition (EMT); miR-429; CRC tumorigenesis; Onecut2
Affiliations: Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Changsha, Hunan, People's Republic of China.

Abstract:  The 5-year survival rate for colorectal cancer is approximately 55 % because of its invasion and metastasis. The epithelial-mesenchymal transition (EMT) is one of the well-defined processes during the invasion and distant metastasis of primary epithelial tumors. miR-429, a member of the miR-200 family of microRNAs, was previously shown to inhibit the expression of transcriptional repressors ZEB1/delta EF1 and SIP1/ZEB2, and regulate EMT. In this study, we showed that miR-429 was significantly downregulated in colorectal carcinoma (CRC) tissues and cell lines. We found that miR-429 inhibited the proliferation and growth of CRC cells in vitro and in vivo, suggesting that miR-429 could play a role in CRC tumorigenesis. We also showed that downregulation of miR-429 may contribute to carcinogenesis and the initiation of EMT of CRC by targeting Onecut2. Further researches indicated that miR-429 inhibited the cells migration and invasion and reversed TGF-β-induced EMT changes in SW620 and SW480 cells. miR-429 could reverse the change of EMT-related markers genes induced by TGF-β1, such as E-cadherin, CTNNA1, CTNNB1, TFN, CD44, MMP2, Vimentin, Slug, Snail, and ZEB2 by targeting Onecut2. Taken together, our data showed that transcript factor Onecut2 is involved in the EMT, migration and invasion of CRC cells; miR-429 inhibits the initiation of EMT and regulated expression of EMT-related markers by targeting Onecut2; and miR-429 or Onecut2 is the important therapy target for CRC. 

Retracted: No

PubPeer comments:
 half of the panels in Figure 4 are duplicated elsewhere in the figure ![file] , 
 #1 Added one more of the images matching those marked in red. No guarantees that there arenu2019t more. *** ![file] ,
Slug down-regulation by RNA interference inhibits invasion growth in human esophageal squamous cell carcinoma
Authors: Kejun Zhang
Shaoyan Zhang
Peng Tang
Zhentao Yu
Yu Wang
Yanbing Zhou
Zhongliang Ma
Dong Chen
Journal: BMC Gastroenterology (2011)
Discipline: CLINICAL MEDICINE
Keywords: Esophageal squamous cell carcinoma; Slug; invasion; apoptosis; metastasis
Affiliations: Department of Surgery, QingDao University, QingDao, Shan Dong Province, People's Republic of China.

Abstract:  Background: Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive carcinomas of the gastrointestinal tract. We assessed the relevance of Slug in measuring the invasive potential of ESCC cells in vitro and in vivo in immunodeficient mice. Methods: We utilized RNA interference to knockdown Slug gene expression, and effects on survival and invasive carcinoma were evaluated using a Boyden chamber transwell assay in vitro. We evaluated the effect of Slug siRNA-transfection and Slug cDNA-transfection on E-cadherin and Bcl-2 expression in ESCC cells. A pseudometastatic model of ESCC in immunodeficient mice was used to assess the effects of Slug siRNA transfection on tumor metastasis development. Results: The EC109 cell line was transfected with Slug-siRNA to knockdown Slug expression. The TE13 cell line was transfected with Slug-cDNA to increase Slug expression. EC109 and TE13 cell lines were tested for the expression of apoptosis-related genes bcl-2 and metastasis-related gene E-cadherin identified previously as Slug targets. Bcl-2 expression was increased and E-cadherin was decreased in Slug siRNA-transfected EC109 cells. Bcl-2 expression was increased and E-cadherin was decreased in Slug cDNA-transfected TE13 cells. Invasion of Slug siRNA-transfected EC109 cells was reduced and apoptosis was increased whereas invasion was greater in Slug cDNA-transfected cells. Animals injected with Slug siRNA-transfected EC109 cells exhibited fewer seeded nodes and demonstrated more apoptosis. Conclusions: Slug down-regulation promotes cell apoptosis and decreases invasion capability in vitro and in vivo. Slug inhibition may represent a novel strategy for treatment of metastatic ESCC. 

Retracted: Yes

PubPeer comments:
 Supplemental Fig. 2a vs Supplemental Fig. 3a. Bands more similar than expected. Could the authors check it? ![file] , 
 Hmm, very interesting. I agree, the panels look the same. I checked the original illustrator files and the U6 panels are as above in all the previous versions of figures that I had saved. It is unfortunate that we or the reviewers didnt notice this during the editorial stage of this paper. ,
Acceleration of epithelial cell syndecan-1 shedding by anthrax hemolytic virulence factors
Authors: Bryan Millis
Charles Bailey
Serguei G Popov
Vikas Chandhoke
Taissia G Popova
Svetlana Nazarenko
Chris Bradburne
Journal: BMC Microbiology (2006)
Discipline: MICROBIOLOGY
Keywords: Staphylococcus aureus; Pseudomonas aeruginosa; Syndecan-1; shedding; B. anthracis
Affiliations: National Center for Biodefense and Infectious Diseases, George Mason University, Manassas, VA 20110, USA. 

Abstract:  Background: It has been recently reported that major pathogens Staphylococcus aureus and Pseudomonas aeruginosa accelerate a normal process of cell surface syndecan-1 (Synd1) ectodomain shedding as a mechanism of host damage due to the production of shedding-inducing virulence factors. We tested if acceleration of Synd1 shedding takes place in vitro upon treatment of epithelial cells with B. anthracis hemolysins, as well as in vivo during anthrax infection in mice. Results: The isolated anthrax hemolytic proteins AnlB (sphingomyelinase) and AnlO (cholesterol-binding pore-forming factor), as well as ClnA (B. cereus homolog of B. anthracis phosphatidyl choline-preferring phospholipase C) cause accelerated shedding of Synd1 and E-cadherin from epithelial cells and compromise epithelial barrier integrity within a few hours. In comparison with hemolysins in a similar range of concentrations, anthrax lethal toxin (LT) also accelerates shedding albeit at slower rate. Individual components of LT, lethal factor and protective antigen are inactive with regard to shedding. Inhibition experiments favor a hypothesis that activities of tested bacterial shedding inducers converge on the stimulation of cytoplasmic tyrosine kinases of the Syk family, ultimately leading to activation of cellular sheddase. Both LT and AnlO modulate ERK1/2 and p38 MAPK signaling pathways, while JNK pathway seems to be irrelevant to accelerated shedding. Accelerated shedding of Synd1 also takes place in DBA/2 mice challenged with Bacillus anthracis (Sterne) spores. Elevated levels of shed ectodomain are readily detectable in circulation after 24 h. Conclusion: The concerted acceleration of shedding by several virulence factors could represent a new pathogenic mechanism contributing to disruption of epithelial or endothelial integrity, hemorrhage, edema and abnormal cell signaling during anthrax infection. 

Retracted: No

PubPeer comments:
 Figure 6. * Boxes of the same color highlight lanes that look remarkably similar. Reported to the journal in July 2015, but no action as of today. ![file] ,
P38 MAPK inhibition protects against glutamate neurotoxicity and modifies NMDA and AMPA receptor subunit expression
Authors: Graciela Gudiño-Cabrera
Antoni Camins
Ruben Darío Castro-Torres
Alfredo I Feria y Velasco
Carlos Beas-Zárate
Martha Catalina Rivera-Cervantes
Rolando Castañeda-Arellano
Journal: Journal of Molecular Neuroscience (2015)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: NMDA receptors; AMPA receptors; excitotoxicity; neonatal treatment; monosodium glutamate
Affiliations: Laboratorio de Neurobiología Celular, Universidad de Guadalajara, Zapopan, Jal, Mexico.

Abstract:  NMDA and AMPA receptors are thought to be responsible for Ca(++) influx during glutamate-induced excitotoxicity and, therefore, hippocampal neuronal death. We assessed whether excitotoxicity induced by neonatal treatment with monosodium glutamate in rats at postnatal age of 1, 3, 5, and 7 modifies the hippocampal expression of the NMDAR subunit NR1 and the AMPAR subunits GluR1/GluR2 at postnatal days 8, 10, 12, and 14. We also assessed the involvement of MAPK signaling by using the p38 inhibitor SB203580. Our results showed that monosodium glutamate induces neuronal death and alters the expression of the subunits evaluated in the hippocampus at all ages studied, which could be prevented by SB203580 treatment.Furthermore, expression of the NRSF gene silencing factor also increased in response to excitotoxicity, suggesting a relationship in suppressing GluR2-expression, which was regulated by the p38-MAPK pathway inhibitor SB203580. This result suggests that selectively blocking the pro-death signaling pathway may reduce neuronal death in some neurodegenerative diseases in which these neurotoxic processes are present and produce major clinical benefits in the treatment of these pathologies. 

Retracted: No

PubPeer comments:
 One band in Figure 6A appears to have a splice (cyan arrow) which is not visible in the others. Do the authors still have access to the original data? *** ![file] , 
 The left panel of Figure 6A may also have a repeated lane and some other possible splices. The uncropped scans would be very helpful. *** Inverse ![file] ,
Cdc42 expression in cervical cancer and its effects on cervical tumor invasion and migration
Authors: Zijian Li
Li Geng
Hongnan Ye
Youyi Zhang
Journal: International Journal of Oncology (2015)
Discipline: CLINICAL MEDICINE
Keywords: Cdc42 expression; cervical cancer; invasion; migration capability; immunohistochemistry
Affiliations: Department of Gynecology and Obstetrics, Peking University Third Hospital, Beijing 100191, P.R. China., Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptide, Ministry of Health, Beijing 100191, P.R. China.

Abstract:  The aim of the present study was to examine Cdc42 expression in cervical cancer and explore its effects on invasion and migration capability of cervical cancer cells. Immunohistochemistry was used to detect Cdc42 expression in normal cervical tissues as well as CIN I or below, CIN II or above, and cervical cancer tissues. Western blot analysis was used to explore Cdc42 expression in normal cervical cell line Crl-2614 and cervical cancer cell line HeLa. Plasmids of constitutively active Cdc42 (Cdc42 CA), wild-type Cdc42 (Cdc42 WT) and dominant negative Cdc42 (Cdc42 DN) were transfected, respectively, into HeLa cells to investigate the impacts of Cdc42 on migration and invasion of cervical cancer cells using Transwell and on cytoskeleton microfilaments using confocal microscopy after immunofluorescence staining. Cdc42 expression was gradually increased in the order of cervical tissues with CIN I or below, CIN II or above and cancer, showing significant difference (P&lt;0.05), and was significantly higher in HeLa cells than in Crl-2614 cells (P&lt;0.05). Migration ability of HeLa cells transfected with Cdc42 CA was significantly higher than that of non-transfected, as well as Cdc42 WT- or Cdc42 DN-transfected HeLa cells (P&lt;0.05). Overexpression of Cdc42 CA can promote filopodia formation in HeLa cells. We concluded that Cdc42 overexpression significantly improved the ability of cervical cancer cells to migrate possibly due to improved pseudopodia formation. 

Retracted: No

PubPeer comments:
 Figure 3. * Yellow boxes: Panels A and E look remarkably similar * Red boxes: Panels B and C look remarkably similar ![file] ,
TMS SMART – Scalp mapping of annoyance ratings and twitches caused by Transcranial Magnetic Stimulation
Authors: Lotte Meteyard
Nicholas P Holmes
Journal: Journal of Neuroscience Methods (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Control conditions; Experimental control; Peripheral effects; TMS; TMS side-effects.
Affiliations: School of Psychology and Clinical Language Sciences, University of Reading, Whiteknights, RG6 6AL, United Kingdom. Electronic address: ., School of Psychology, University Park, University of Nottingham, Nottingham, NG7 2RD, United Kingdom. Electronic address: .

Abstract:  Background: The magnetic pulse generated during transcranial magnetic stimulation (TMS) also stimulates cutaneous nerves and muscle fibres, with the most commonly reported side effect being muscle twitches and sometimes painful sensations. These sensations affect behaviour during experimental tasks, presenting a potential confound for 'online' TMS studies. New method: Our objective was to systematically map the degree of disturbance (ratings of annoyance, pain, and muscle twitches) caused by TMS at 43 locations across the scalp. Ten participants provided ratings whilst completing a choice reaction time task, and ten different participants provided ratings whilst completing a 'flanker' reaction time task. Results: TMS over frontal and inferior regions resulted in the highest ratings of annoyance, pain, and muscle twitches caused by TMS. We predicted the difference in reaction times (RT) under TMS by scalp location and subjective ratings. Frontal and inferior scalp locations showed the greatest cost to RTs under TMS (i.e., slowing), with midline sites showing no or minimal slowing. Increases in subjective ratings of disturbance predicted longer RTs under TMS. Critically, ratings were a better predictor of the cost of TMS than scalp location or scalp-to-cortex distance. The more difficult 'flanker' task showed a greater effect of subjective disturbance. Comparison with existing methods: We provide the data as an online resource (www.tms-smart.info) so that researchers can select control sites that account for the level of general interference in task performance caused by online single-pulse TMS. Conclusions: The peripheral sensations and discomfort caused by TMS pulses significantly and systematically influence RTs during single-pulse, online TMS experiments. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: With Dr Lotte Meteyard, we planned funded this small, 1-experiment project. It should have been on 100 subjects with both hemispheres an MRI scan each. Instead it was N=20, one hemisphere, and no scan. We needed more resources (time, money, staff) to do justice to this project. ,
Long noncoding RNA HOTTIP alleviates oxygen‐glucose deprivation‐induced neuronal injury via modulating miR‐143/hexokinase 2 pathway
Authors: Jianping Lv
Guoce Li
Li Zhao
Yan Wang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: glycolytic metabolism; hexokinase 2; ischemic stroke; long noncoding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP); miR-143.
Affiliations: Department of Neurology Cangzhou Central Hospital Cangzhou City Hebei Province China

Abstract:  HOXA transcript at the distal tip (HOTTIP), which is a long noncoding RNA, plays an important role in multiple cancers and in coronary artery disease. Elevated microRNA-143 (miR-143) expression causes impaired glucose uptake that is responsible for the ischemic cerebral injury. However, the role and mechanism of HOTTIP in ischemic stroke are still unknown. The expression of HOTTIP and miR-143 was first detected in mouse models of transient middle cerebral artery occlusion and in primary neurons exposed to oxygen-glucose deprivation (OGD). We used gain-of function and loss-of function approaches in vitro to investigate the effect and mechanism of HOTTIP on ischemic stroke by evaluating cell viability, apoptosis, and glycolytic metabolism of neurons exposed to OGD. The HOTTIP expression was decreased, whereas miR-143 increased in experimental ischemic stroke models. Overexpression of HOTTIP by the pcDNA3.1-HOTTIP plasmid significantly increased cell viability, glucose uptake, and the expression of hexokinase 2 (HK-2) and pyruvate kinase M2 that were reduced by OGD insult. The HOTTIP overexpression also diminished OGD induced the apoptosis and the caspase-3 activity of neurons. The miR-143 mimic reversed these effects, and anti-miR-143 enhanced them. In addition, we found that HOTTIP could function as a competing endogenous RNA for miR-143 to modulate HK-2 expression. In conclusion, the HOTTIP expression was reduced in ischemic stroke. The HOTTIP overexpression attenuated OGD-induced neuronal injury and imbalanced glycolytic metabolism by sponging miR-143, resulting in the de-repression of its endogenous target HK-2. Taken together, these findings improve understanding of the pathogenesis of ischemic stroke. 

Retracted: No

PubPeer comments:
 Fig 2C,  The apoptosis of neurons was analyzed by flow cytometry ; and 4B,  The apoptosis of neurons was analyzed by flow cytometry . The resolution is not high. ![file] I have color-coded three panels with orange, pink, bright pink boxes to highlight similarities to panels from Fig 2(a) of [Zhang (2019)] . ![] Bright pink panel also appears in Fig 3A of [Long et al (2017)] . ![] Orange, pink panels also appear in Fig 2C of [Li et al (2016)] . ![] , 
 Fig 2C again, with light blue box added. ![file] Fig 2B of [Meng et al (2017)] , 2B of [Wang et al (2017)] , and Fig 2C of [Li et al (2016)] . Light-blue overlap is only partial, and Q3 appears to have been reworked. ![] ![] ![] ,
RAS promotes tumorigenesis through genomic instability induced by imbalanced expression of Aurora-A and BRCA2 in midbody during cytokinesis
Authors: Asha S Multani
Imelda Mercado-Uribe
Gong Yang
Kwong-Kwok Wong
Subrata Sen
Ie-Ming Shih
David M Gershenson
Jinsong Liu
Journal: International Journal of Cancer (2013)
Discipline: CLINICAL MEDICINE
Keywords: oncogene; RAS; genomic instability; cancer development; Aurora-A
Affiliations: Cancer Research Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China. , Department of Pathology; The University of Texas MD Anderson Cancer Center; Houston; TX, Department of Genetics; The University of Texas MD Anderson Cancer Center; Houston; TX, Department of Molecular Pathology; The University of Texas MD Anderson Cancer Center; Houston; TX, Department of Gynecologic Pathology; School of Medicine; The Johns Hopkins University; Baltimore; MD, Department of Gynecological Oncology; The University of Texas MD Anderson Cancer Center; Houston; TX

Abstract:  The oncogene RAS is known to induce genomic instability, leading to cancer development; the underlying mechanism, however, remains poorly understood. To better understand how RAS functions, we measured the activity of the functionally related genes Aurora-A and BRCA2 in ovarian cancer cell lines and tumor samples containing RAS mutations. We found that Aurora-A and BRCA2 inversely controlled RAS-associated genomic instability and ovarian tumorigenesis through regulation of cytokinesis and polyploidization. Overexpression of mutated RAS ablated BRCA2 expression but induced Aurora-A accumulation at the midbody, leading to abnormal cytokinesis and ultimately chromosomal instability via polyploidy in cancer cells. RAS regulates the expression of Aurora-A and BRCA2 through dysregulated protein expression of farnesyl protein transferase β and insulin-like growth factor binding protein 3. Our results suggest that the imbalance in expression of Aurora-A and BRCA2 regulates RAS-induced genomic instability and tumorigenesis. 

Retracted: No

PubPeer comments:
 July 2015 correction, https: onlinelibrary.wiley.com doi full 10.1002 ijc.29553 It reads:  The image of BRCA2 staining (Figure 2b upper right) indicated from the tumor with KRAS mutation was erroneously taken from that with BRAF mutation during final figure preparation. The corrected Figure 2b showing BRCA2 staining (Figure 2b upper right) from the tumor with KRAS mutation is now provided, while the figure legend remains unchanged. The corrected figure is shown below. The authors apologize for the error. Here is the original Figure 2B as reported to the journal, with red boxes showing a region of overlap. I thank the authors and journal staff for correcting this error. ![file] ,
Massively Parallel Single Nucleus Transcriptional Profiling Defines Spinal Cord Neurons and Their Activity during Behavior
Authors: Ariel J Levine
Matthew W Kelley
Kory R Johnson
Tzipporah B Bergman
Michael C Kelly
Kaya J E Matson
Anna R Ryba
Courtney I Dobrott
Li Li
Anupama Sathyamurthy
Journal: Cell Reports (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: neuronal activity; single cell RNA-seq; snRNA-seq; spinal cord.

Abstract:  To understand the cellular basis of behavior, it is necessary to know the cell types that exist in the nervous system and their contributions to function. Spinal networks are essential for sensory processing and motor behavior and provide a powerful system for identifying the cellular correlates of behavior. Here, we used massively parallel single nucleus RNA sequencing (snRNA-seq) to create an atlas of the adult mouse lumbar spinal cord. We identified and molecularly characterized 43 neuronal populations. Next, we leveraged the snRNA-seq approach to provide unbiased identification of neuronal populations that were active following a sensory and a motor behavior, using a transcriptional signature of neuronal activity. This approach can be used in the future to link single nucleus gene expression data with dynamic biological responses to behavior, injury, and disease. 

Retracted: No

PubPeer comments:
 One of the first study to provide extensive data about gene expression in the clusters of spinal cord neurons in the dorsal spinal cord: 16 populations of excitatory interneurons, 9 clusters of Inhibitory interneurons in the medial spinal cord: 1 populations of excitatory interneurons, 4 groups of Inhibitory interneurons in the ventral spinal cord: 4 populations of excitatory interneurons, 5 groups of Inhibitory interneurons, 2 groups of cholinergic neurons, 2 group of mixed (excitatory and inhibitory) neurons One of the two Ventral Cholinergic (VC1) group is putetively identified as the V0c interneurons, the other one (VC2) as the motonuerons ,
Sequence dependence of tRNA(Gly) import into tobacco mitochondria
Authors: Anne-Marie Duchêne
Thalia Salinas
Laurence Maréchal-Drouard
Cécile Schaeffer
Journal: Biochimie (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Plant mitochondrial genomes; tRNA genes; tRNA import; tRNA(Gly) isoacceptors; tobacco mitochondria
Affiliations: Institut de Biologie Moléculaire des Plantes, UPR du CNRS no. 2357, Université Louis Pasteur, 12, rue du Général Zimmer, 67000 Strasbourg, France.

Abstract:  Plant mitochondrial genomes lack a number of tRNA genes and the corresponding tRNAs, which are nuclear-encoded, are imported from the cytosol. We show that specific import of tRNA(Gly) isoacceptors occurs in tobacco mitochondria: tRNA(Gly)(UCC) and tRNA(Gly)(CCC) are cytosolic and mitochondrial, while tRNA(Gly)(GCC) is found only in the cytosol. Exchange of sequences between tRNA(Gly)(UCC) and tRNA(Gly)(GCC) shows that the anticodon and D-domain are essential for tRNA(Gly)(UCC) import. However the reverse mutations in tRNA(Gly)(GCC) are not sufficient to promote its import into tobacco mitochondria. 

Retracted: No

PubPeer comments:
 In Figure 3, a Western immunoblot shows Nrf2 with a MW of 57 kDa. This is wrong. Nrf2 is observed at 95-110 kDa. For more information please see Lau A et al., 2013; Antioxid Redox Signal. 2013 Jan 1;18(1):91-3. doi: 10.1089 ars.2012.4754. The difference in theoretical and observed MW weight for Nrf2 is explained by high content of acidic amino acids. Please see Guan Y et al., 2015; Sci Rep. 2015 Aug 27;5:13370. doi: 10.1038 srep13370. In this paper they have compared several proteins with high content of acidic amino acids, all of which show reduced migration in Western immunoblotting. , 
 There are additional inconsistencies in the Western blots. The methods never mention loading controls, yet gels are displayed with beta-actin and GAPDH controls. It may be that the authors forgot to report this in their methods. However, it is curious that a number of these loading controls seem to be virtually identical. No matter whether they are reported as beta-actin or GAPDH. ![file] There is also an issue with the histological scores. Given that scores were 0, 1, 2, or 3 for each subject, these data are problematic. ![file] Not only are the error bars miniscule for this type of data, the data presented for the TAA group is impossible. The only way the group can average a score of 3 is if all subjects were scored a 3. But at this point the standard error of data would be zero. Something is wrong here. I would strongly urge the authors to look into what may have caused these problems in data. ,
RETRACTED ARTICLE: Nanoformulation of Apolipoprotein E3-Tagged Liposomal Nanoparticles for the co-Delivery of KRAS-siRNA and Gemcitabine for Pancreatic Cancer Treatment
Authors: Fengyong Wang
Zhen Zhang
Journal: Pharmaceutical Research (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: E3-based liposomes; Gemcitabine; KRAS; Pancreatic cancer; RNA interference.
Affiliations: Department of General Surgery, Tongde Hospital of Zhejiang Province, Hangzhou, 310012, Zhejiang Province, China., Department of General Surgery, Tongde Hospital of Zhejiang Province, Hangzhou, 310012, Zhejiang Province, China. .

Abstract:  Purpose: KRAS is the most frequently mutated gene in human cancers, and ~ 90% of pancreatic cancers exhibit KRAS mutations. Despite the well-known role of KRAS in malignancies, directly inhibiting KRAS is challenging. Methods: In this study, we successfully synthesized apolipoprotein E3-based liposomes for the co-delivery of gemcitabine (GEM) and a small interfering RNA targeting KRAS (KRAS-siRNA) to improve the efficacy of pancreatic cancer treatment. Results: Apolipoprotein E3 self-assembly on the liposome surface led to a substantial increase in its internalization in PANC1 human pancreatic cancer cells. KRAS-siRNA led to downregulated KRAS protein expression and KRAS-dependent carcinogenic pathways, resulting in the inhibition of cell proliferation, cell cycle arrest, increased apoptosis, and suppression of tumor progression. The combination of KRAS-siRNA and GEM induced a synergistic improvement in cell apoptosis and significantly lower cell viability compared with single-agent therapy. The low IC50 value of A3-SGLP might be attributed to potentiation of the anticancer effect of GEM by siRNA-mediated silencing of KRAS mutations, thereby inducing synergistic effects on cancer cells. Conclusion: A3-SGLP led to a marked decrease in the overall tumor burden and did not show any signs of toxicity. Therefore, the combination of KRAS-siRNA and GEM holds great potential for the treatment of pancreatic cancer. 

Retracted: Yes

PubPeer comments:
 A part of the reference list is attached. 34 out of the total 85 cited papers are authored by G.W. Wei and his co-authors. ![file] ![file] , 
 The title of this paper suggests that this paper is about u201c**M-fuzzifying geometric interval space**u201d. However, the abstract reads u201cIn this paper, we investigate the **multiple attribute decision making problems with Pythagorean fuzzy information**u201d The whole paper has nothing to do with u201c**M-fuzzifying geometric interval space**u201d. , 
 See also an identical 2019 paper in the same journal on https: pubpeer.com publications A21F9BE731F3816D4B323E2991B14E ,
Cell phenotype-specific down-regulation of Smad3 involves decreased gene activation as well as protein degradation
Authors: Ruoyun Tan
Anne-Christine Poncelet
Youhua Liu
Constance E Runyan
H William Schnaper
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Transforming growth factor-beta; TGF-beta; Smad proteins; renal fibrosis; ubiquitination
Affiliations: Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98109, USA. 

Abstract:  Signaling by transforming growth factor-beta (TGF-beta), a regulator of several biological processes, including renal fibrosis, is mediated, in part, by the Smad proteins. Tight control of Smad level and activity is critical for proper TGF-beta biological functions. Here, we have investigated the mechanisms involved in regulating Smad3 expression. In human glomerular mesangial cells, Smad3 protein levels were specifically reduced by 24 h of TGF-beta1 treatment, whereas Smad2 and Smad4 levels were not. TGF-beta1 increased endogenous Smad3 ubiquitination, and proteasome inhibitor treatment blocked TGF-beta1-mediated Smad3 down-regulation resulting in accumulation of ubiquitinated Smad3. These data support the concept that Smad3 down-regulation occurs via degradation by the ubiquitin/proteasome machinery. However, changes in Smad3 protein levels were also paralleled by changes in Smad3 mRNA expression. TGF-beta1 did not decrease Smad3 mRNA stability, but it significantly inhibited Smad3 promoter activity. In renal tubular epithelial cells, decreased Smad3 levels were observed only after exposure to TGF-beta1 for longer time periods (5-7 days) that paralleled epithelial-to-mesenchymal transition, as determined by increased expression of smooth muscle alpha-actin and decreased expression of E-cadherin. Decline in Smad3 expression also occurred in kidneys after unilateral ureteral obstruction, a model of tubulointerstitial fibrosis associated with TGF-beta up-regulation and epithelial-to-mesenchymal transition. Our data show for the first time that TGF-beta1 modulates the expression of a receptor-activated Smad at both the protein and transcriptional level. Smad3 down-regulation could represent a feedback loop controlling TGF-beta signaling in a cell phenotype-specific manner. 

Retracted: No

PubPeer comments:
 The immunoblot for Smad4 of different groups in red boxes appear to look similar in Fig 1A and 2. ![file] ,
Overexpression of UBE2C correlates with poor prognosis in gastric cancer patients
Authors: B Ke
L-R Liu
X-S Hao
H-Q Zhang
G Zhao
G Ma
H Liang
G-L Liu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: UBE2C; gastric cancers; expression; overall survival rate; Real-time PCR
Affiliations: Department of Gastrointestinal Cancer Biology, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China. .

Abstract:  Objective: The ubiquitin-conjugating enzyme E2C (UBE2C) has been known as a crucial factor upregulated in various tumors. The functions of UBE2C is mainly involved in the pathway protein ubiquitination. This study investigates the expression of UBE2C in gastric cancers and its correlation with overall survival rate. Materials and methods: Real-time PCR (RT-PCR) and Western blotting were performed to determine the expression of UBE2C in gastric cancer samples and adjacent normal tissues. Immunohistochemical staining was used to assess the expression of UBE2C in 216 paraffin-embedded gastric cancer tissues. Results: The mRNA and relevant protein levels of UBE2C in gastric cancer tissues are significantly greater than those in the adjacent normal tissues. Also, the expression of UBE2C is found to correlate with lymphatic metastasis, serosa invasion, TNM (Malignant Tumors) staging and Lauren's classification (p&lt;0.05). The univariate analysis shows that the overexpression of UBE2C associates with poor prognosis (p=0.001). The multivariate analysis demonstrates that expression of UBE2C, lymphatic metastasis, and TNM staging are independent prognostic indicators. Conclusions: This study shows that overexpression of UBE2C contributes to the development of gastric cancer, and UBE2C has the potential to be exploited as a therapeutic target. 

Retracted: No

PubPeer comments:
 Something went wrong with Figure 2. Maybe the authors can have it corrected? ![file] ,
FOXP3 is an X-linked breast cancer suppressor gene and an important repressor of the HER-2/ErbB2 oncogene
Authors: Lizhong Wang
Weiquan Li
Xing Chang
Virginia Godfrey
Tianyu Yang
Chang-Gong Liu
Tim H-M Huang
Carl Morrison
Michael W Y Chan
Bae Keun Park
Xingluo Liu
Richard Love
Jin-Qing Liu
Pan Zheng
Huiming Zhang
Yin Wang
Yang Liu
Yan Liu
Rulong Shen
Cun-Yu Wang
Tao Zuo
Journal: Cell (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Foxp3; cancer; breast cancer; HER-2/ErbB2; transcription factor
Affiliations: Program in Molecular, Cellular, and Developmental Biology and Department of Molecular Virology, Immunology, and Medical Genetics, Ohio State University Medical Center and Comprehensive Cancer Center, Columbus, OH 43210, USA.

Abstract:  The X-linked Foxp3 is a member of the forkhead/winged helix transcription factor family. Germline mutations cause lethal autoimmune diseases in males. Serendipitously, we observed that female mice heterozygous for the "scurfin" mutation of the Foxp3 gene (Foxp3(sf/+)) developed cancer at a high rate. The majority of the cancers were mammary carcinomas in which the wild-type Foxp3 allele was inactivated and HER-2/ErbB2 was overexpressed. Foxp3 bound and repressed the HER-2/ErbB2 promoter. Deletion, functionally significant somatic mutations, and downregulation of the FOXP3 gene were commonly found in human breast cancer samples and correlated significantly with HER-2/ErbB2 overexpression, regardless of the status of HER-2 amplification. Our data demonstrate that FOXP3 is an X-linked breast cancer suppressor gene and an important regulator of the HER-2/ErbB2 oncogene. 

Retracted: No

PubPeer comments:
null, 
 Here is the original, yet-uncorrected Figure 7, with the duplicated panels in Figure 7A that were corrected in the erratum marked in blue. Unfortunately, three other panels that appear duplicated with panels in Figure 7D have not yet been corrected. Note that plates are shown upside down, so 180 degrees rotated, so these are not simple duplications as the one that was corrected. Could the authors please check if these three additional marked plates have been duplicated too? ![file] ,