PReD-Bench/PRed-Bench huggingface dataset:
Inactivating mutations of caspase-8 gene in colorectal carcinomas
Authors: Seong Whan Jeong
Jong Woo Lee
Nam Jin Yoo
Hong Sug Kim
Suk Woo Nam
Chang Jae Kim
Sug Hyung Lee
Youg Gu Cho
Won Sang Park
Jung Young Lee
Jik Young Park
Young Hwa Soung
Jong Heun Lee
Su Young Kim
Sang Ho Kim
Journal: Gastroenterology (2003)
Discipline: CLINICAL MEDICINE
Keywords: apoptosis; caspase-8; mutation; colorectal cancer; carcinomas

Abstract:  Background &amp; aims: There has been evidence that dysregulation of apoptosis is involved in the pathogenesis of cancer development. Caspase-8 is an initiation caspase that activates the caspase cascade during apoptosis. The aim of this study was to explore the possibility that mutation of the caspase-8 gene might be involved in the development of colorectal cancer. Methods: We analyzed the entire coding region of the caspase-8 gene for the detection of somatic mutations in 180 colorectal tumors (98 invasive carcinomas and 82 adenomas) by polymerase chain reaction, single-strand conformation polymorphism, and DNA sequencing. Results: Overall, we detected a total of 5 somatic mutations in 98 invasive carcinomas (5.1%), but no mutations were detected in 82 adenomas (0%). The frequency of caspase-8 mutation in the carcinomas was significantly higher than that in adenomas (P &lt; 0.05). The 5 mutations consisted of 1 frameshift, 1 nonsense mutation, and 3 missense mutations. We expressed the 5 tumor-derived caspase-8 mutants and found that 3 of the 5 mutations markedly decreased apoptosis activity of caspase-8. Furthermore, expression of the inactivating caspase-8 mutants interfered with apoptosis by death receptor overexpression, indicating that these mutants have dominant-negative inhibition of the death receptor-induced apoptosis. Conclusions: The presence of caspase-8 mutation in colon carcinomas suggests that caspase-8 gene mutation might lead to the loss of its apoptotic function and contribute to the pathogenesis of colorectal carcinomas, especially at the late stage of colorectal carcinogenesis. 

Retracted: No

PubPeer comments:
 I am the corresponding author of this paper. As I reviewed our earlier publication, I accidentally found that there was an error in this paper. In figure 1, we inserted two cases of caspase-8 mutation (nucleotide 1237 and 1238), but the normal sequence (not the cancer-specific mutations) are reused without the notification. Although they were normal DNA sequences that must be equal from the SSCP finding, we should have used different sequencing gels. The student might not understand the importance of data usage and also as a corresponding author I should have checked the original gels. While we feel sorry that we report the error, we feel relived that the error is known through this site. Thank you.![file] ,
The relevance of NF-kappaB for CD95 signaling in tumor cells
Authors: Bryan C Barnhart
Marcus E Peter
Patrick Legembre
Journal: Cell Cycle (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: death receptor family; CD95; apoptosis; non-apoptotic pathways; NF-kappaB
Affiliations: The Ben May Institute for Cancer Research, Committees on Immunology and Cancer Biology, The University of Chicago, Chicago, Illinios 60637, USA.

Abstract:  Most members of the death receptor family including CD95 (APO-1/Fas) have been shown to induce both apoptosis as well as non-apoptotic pathways depending on the tissue and the circumstances. One of the non-apoptotic pathways emanating from CD95, activation of NF-kappaB, has recently been demonstrated to regulate invasiveness of apoptosis resistant tumor cells. In contrast, activation of NF-kappaB in apoptosing cells is believed to be suppressed due to cleavage of various NF-kappaB pathway components by active caspases that execute apoptosis. We now present data demonstrating that in certain highly CD95 apoptosis sensitive cells NF-kappaB is robustly activated. In fact overexpression of apoptosis inhibitors such as Bcl-2 or c-FLIPL in these cells results in decreased activation of NF-kappaB through CD95. We propose a model in which NF-kappaB is generally activated in certain cells but may have different functions depending on whether cells are programmed to die or to survive. 

Retracted: No

PubPeer comments:
 Posting this comment again as it keeps on bugging (sorry for the redundancy). Several  cuts appear in several panels (Fig1A, 2B, 3B; orange arrows). ![file] , 
 This kind of splicing was allowed and quite common back in 2004. Not done these days anymore. Most journals adopted new image manipulation rules about ten years ago. Some of the splicing is very obvious. It was not done to hide but to look even so not to distract from the data. ,
Over-expression of mir-124 inhibits MMP-9 expression and decreases invasion of renal cell carcinoma cells
Authors: M-C Sun
W-D Gu
H-Z Geng
L-D Zhang
P Wang
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: JAK-STAT3 signaling pathway; MicroRNA-124; renal cell carcinoma; matrix metalloproteinase-9 (MMP-9); STAT3
Affiliations: Department of Urology, Heze Municipal Hospital, Heze, China. .

Abstract:  Objective: JAK-STAT3 signaling pathway is related to tumor invasion and metastasis that can regulate matrix metalloproteinase-9 (MMP-9) expression. MicroRNA-124 (MiR-124) was found downregulated in renal cell carcinoma. Bioinformatics analysis revealed the complementary binding site between miR-124 and 3'-UTR of signal transducers and activators of transcription 3 (STAT3). This study investigated the role of miR-124 in regulating Janus kinase (JAK)-STAT3 activity, MMP-9 expression, and renal cell carcinoma invasion. Materials and methods: Luciferase assay was used to test the targeting regulatory effect of miR-124 on STAT3. MiR-124, STAT3, phosphorylated STAT3 (p-STAT3), and MMP-9 expressions were compared in HK-2, 769-P, and OS-RC-2 cells. Transwell assay was applied to evaluate cell invasion. OS-RC-2 cells were divided into control, miR-NC, miR-124 mimic, STAT3 inhibition, and miR-124 mimic+Stattic groups. Results: MiR-124 targeted inhibited STAT3 expression. OS-RC-2 cells exhibited the strongest invasive ability, followed by 769-P and HK-2 cells. STAT3, p-STAT3, and MMP-9 expressions were highest in OS-RC-2 cells, followed by 769-P and HK-2 cells. MiR-124 demonstrated the opposite expression trend. MiR-124 mimic and/or Stattic treatment attenuated cell invasion through reducing STAT3, p-STAT3, and MMP-9 levels. Conclusions: MiR-124 down-regulation was associated with renal cancer cell OS-RC-2 invasion enhancement. Over-expression of miR-124 attenuated OS-RC-2 cell invasion by down-regulating STAT3 and MMP-9. 

Retracted: No

PubPeer comments:
 This paper has features suggestive of [what has elsewhere been labeled as  Papermill #2 ] , characterised by stylised geometrical WBs that are reduced to sharp-edged black blobs ovals on a featureless grey background, reminiscent of a Miro painting: ![file] ![file] Other examples are listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit?usp=sharing , 
 Fig 2B,  Transwell assay detection of [OS-RC-2] invasive ability ... ![file] ... and Fig 3C,  Transwell assay detection of cell invasion . ![file] Unexpected overlaps with Figure 4 of [Zhang et al (2019)] .  Transfection of miR-199 mimic significantly attenuated the invasion of MHCC97H cells. ![file] As a corollary, Figs 2B and 3C overlap directly, but that is the least of the concerns here. , 
 #2 Fig 3C again. ![] Fig 3D from [Zhang et al (2017)] . ![file] ,
ZCCHC3 is a co-sensor of cGAS for dsDNA recognition in innate immune response
Authors: Yun-Da Chen
Yu-Zhi Fu
Wen Ye
Cao-Qi Lei
Xia-Nan Zhang
Wei-Wei Luo
Ru Zang
Shu Li
Ming-Ming Hu
Huan Lian
Qing Yang
Jin Wei
Hong-Bing Shu
Journal: Nature Communications (2018)
Discipline: Multidisciplinary
Keywords: cGAS; ZCCHC3; dsDNA; DNA virus; innate antiviral response
Affiliations: Medical Research Institute, School of Medicine, Wuhan University, 430071, Wuhan, China., College of Life Sciences Wuhan University, 430072, Wuhan, China., Wuhan Institute of Virology, Chinese Academy of Sciences, 430071, Wuhan, China., Medical Research Institute, School of Medicine, Wuhan University, 430071, Wuhan, China. ., College of Life Sciences Wuhan University, 430072, Wuhan, China. .

Abstract:  Cyclic GMP-AMP synthase (cGAS) senses double-strand (ds) DNA in the cytosol and then catalyzes synthesis of the second messenger cGAMP, which activates the adaptor MITA/STING to initiate innate antiviral response. How cGAS activity is regulated remains enigmatic. Here, we identify ZCCHC3, a CCHC-type zinc-finger protein, as a positive regulator of cytosolic dsDNA- and DNA virus-triggered signaling. We show that ZCCHC3-deficiency inhibits dsDNA- and DNA virus-triggered induction of downstream effector genes, and that ZCCHC3-deficient mice are more susceptible to lethal herpes simplex virus type 1 or vaccinia virus infection. ZCCHC3 directly binds to dsDNA, enhances the binding of cGAS to dsDNA, and is important for cGAS activation following viral infection. Our results suggest that ZCCHC3 is a co-sensor for recognition of dsDNA by cGAS, which is important for efficient innate immune response to cytosolic dsDNA and DNA virus. 

Retracted: No

PubPeer comments:
 #1 This is Huan Lian, the first author of this paper. The primers for GAPDH are correct, there is just a typo in the sequence of the primer. GAGTCAACGGATTTGGTcGT GAGTCAACGGATTTGGTgGT We didn t use Gbp1 primers to perform any Gbp1-related experiments in this paper. , 
 According to In-Silico PCR result, primers for GAPDH showed no amplification, and primers for Gbp1 showed amplification of Gbp2. Could authors give an explanation? ![file] ,
Cryopreservation of Brassidium Shooting Star orchid using the PVS3 method supported with preliminary histological analysis
Authors: Safiah Ahmad Mubbarakh
Nazrin Nadirah Mohd Sah
Safrina Rahmah
Sreeramanan Subramaniam
Zuraida Abdul Rahman
Journal: Applied biochemistry and biotechnology (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cryopreservation; Brassidium Shooting Star orchid; PLBs; PVS3 vitrification method; viability assessment
Affiliations: School of Biological Sciences, Universiti Sains Malaysia, 11800, Gelugor, Penang, Malaysia.

Abstract:  Cryopreservation is an alternative, safe, and cost-effective method for long-term plant genetic resource conservation. This study was conducted to optimize the conditions for cryopreserving the protocorm-like bodies (PLBs) of Brassidium Shooting Star orchid with the PVS3 vitrification method. Five parameters were assessed in this study: PLB size, sucrose concentration, preculture duration, PVS3 duration, and unloading duration. The viability of the cryopreserved PLBs was determined using the triphenytetrazolium chloride assay and growth recovery assessments. The optimum condition for the cryopreservation of the PLBs of Brassidium Shooting Star orchid is based on the size range between 3 and 4 mm precultured with half-strength semi-solid MS media supplemented with 0.25 M sucrose for 24 h, followed by treatment with loading solution mixture of 2 M glycerol and 0.4 M sucrose supplemented with half-strength liquid MS media at 25 °C for 20 min. The PLBs were then dehydrated with PVS3 at 0 °C for 20 min prior to immersion in liquid nitrogen; finally, the PLBs were immersed with half-strength liquid MS media supplemented with 1.2 M sucrose for 30 min. Histological analyses displayed denser cytoplasm and voluminous nucleus in the cryopreserved PLBs of Brassidium Shooting Star orchid. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
 No correction, as promised by the authors 4 years ago, can be found for this article: https: link.springer.com article 10.1007%2Fs12010-013-0597-0 https: www.ncbi.nlm.nih.gov pubmed 24146369 ,
Antidepressant-like effects of 3,6′-disinapoyl sucrose on hippocampal neuronal plasticity and neurotrophic signal pathway in chronically mild stressed rats
Authors: Khalid Rahman
Ping Liu
Guo Dai-Hong
Hong-Bo Liao
Yu-Yu Wang
Yuan Hu
Journal: Neurochemistry International (2010)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: antidepressant treatment; hippocampal neuronal plasticity; neurogenesis; 3,6'-disinapoyl sucrose (DISS); Polygala tenuifolia Willd
Affiliations: Department of Clinical Pharmacology and Pharmacy, Center of Pharmacy, Chinese PLA General Hospital, Beijing 100853, China.

Abstract:  Recent studies suggest that the behavioral effects of chronic antidepressant treatment are mediated by stimulation of hippocampal neuronal plasticity and neurogenesis. The present study was designed to examine the effects of 3,6'-disinapoyl sucrose (DISS), a bioactive component of Polygala tenuifolia Willd, on the expressions of four plasticity-associated genes: cell adhesion molecule L1 (CAM-L1), laminin, cAMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in hippocampus, all of which are involved in neuronal plasticity and neurite outgrowth. We confirmed that chronic stress in rats caused a reduction in sensitivity to reward (sucrose consumption) and a decrease in mRNA levels of CAM-L1, laminin, and BDNF, together with a decrease in protein levels of phosphorylated CREB and BDNF. Repeated administration of DISS for 21 days at doses of 5, 10 and 20mg/kg reversed stress-induced alterations in sucrose consumption and these target mRNA and protein levels. In conclusion, increased expressions in the hippocampus of three noradrenergic-regulated plasticity genes and one neurotrophic factor may be one of the molecular and cellular mechanisms underlying the antidepressant action of DISS in chronic mild stress (CMS) rats. 

Retracted: No

PubPeer comments:
 The same sets of blots appear to show up in three spots across Figures 3 and 4. ![file] There is different amounts of noise on the blots, but the shapes, sizes and relative positions are identical (checked through rescalling and matching). Would the authors happen to have the original uncropped blots for these? Could something have gone wrong here? ,
Hepatocyte Growth Factor Protects against Hypoxia/Reoxygenation-induced Apoptosis in Endothelial Cells
Authors: Yushen Zhou
Hong Pyo Kim
Augustine M K Choi
Ruiping Song
Xue Wang
Stefan W Ryter
Reza Zarnegar
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hypoxia/reoxygenation; cellular injury; cell death pathways; Bax translocation; cytochrome c release
Affiliations: Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA.

Abstract:  Hypoxia/reoxygenation causes cellular injury and death associated with a number of pathophysiological conditions, including myocardial ischemia/reperfusion injury and stroke. The cell death pathways induced by hypoxia/reoxygenation and their underlying regulatory mechanisms remain poorly understood. Recent studies have shown that hypoxia/reoxygenation can induce Bax translocation and cytochrome c release. Using murine lung endothelial cells as a model, we found that the induction of apoptosis by hypoxia/reoxygenation involved the activation of both Bax-dependent and death receptor-mediated pathways. We demonstrated the activation of the death-inducing signal complex and Bid pathway after hypoxia/reoxygenation. Hepatocyte growth factor markedly inhibited hypoxia/reoxygenation-induced endothelial cell apoptosis. The cytoprotection afforded by hepatocyte growth factor was mediated in part by the stimulation of FLICE-like inhibiting protein expression, the attenuation of death-inducing signal complex formation, and the inhibition of Bid and Bax activation. Hepatocyte growth factor also prevented cell injury and death by increasing the expression of the antiapoptotic Bcl-XL protein. The inhibition of Bid/Bax-induced cell death by hepatocyte growth factor primarily involved p38 MAPK and in part Akt-dependent pathways but not ERK1/ERK2. 

Retracted: No

PubPeer comments:
 Figures 2E and 4B. FLIP panels much more similar than expected, although the timings are different. ![file] , 
 #1 Much more similar than expected. ![file] , 
 #2 Correction. ![file] ,
Blocking the PD-1/PD-L1 axis enhanced cisplatin chemotherapy in osteosarcoma in vitro and in vivo
Authors: Hui Xie
Shaoya He
Xiaoqiang Liu
Tao Zhang
Zhongliang Deng
Huaming Wu
Journal: Environmental Health and Preventive Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: Anti-PD-1 antibody; Cisplatin; Osteosarcoma; PD-L1; Treg cell.
Affiliations: Department of Orthopedic Surgery, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Yuzhong district, Chongqing, 40010, China., Department of Orthopedic Surgery, Sichuan Anyue County People's Hospital, 68 Wainan Street, Anyue, 642350, China., Department of Gastroenterology, Sichuan Anyue County People's Hospital, 68 Wainan Street, Anyue, 642350, China., Department of orthopedic Surgery, Guizhou Orthopedics Hospital, 123 Shachong South Road, Guiyang, 550002, China., Department of Orthopedic Surgery, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Yuzhong district, Chongqing, 40010, China. .

Abstract:  Background: The blocking of the programmed cell death protein (PD-1)/programmed death-ligand 1 (PD-L1) axis has been found to have an anticancer activity against various types of cancer by enhancing T cell immunity, while there are no studies linking the PD-1/PD-L1 axis to chemotherapy drugs in osteosarcoma (OS). The present study aimed to investigate the effects of blocking PD-1/PD-L1 axis on the cisplatin chemotherapy in OS in vitro and in vivo. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was applied to detect PD-L1 mRNA in OS tissues. Cell proliferation and apoptosis were measured by Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. In vivo, the syngeneic mice were treated with cisplatin and anti-PD-1 antibody alone or jointly. Results: In this study, it revealed that PD-L1 mRNA was highly expressed in OS tissues. Further inhibitory evaluation showed that the K7M2-LV cells (PD-L1 overexpression) co-cultured with PD-1+ lymphocytes could promote K7M2 cell proliferation. Meanwhile, the combination of anti-PD-1 antibody and cisplatin significantly decreased the proliferation and increased the apoptosis of K7M2 cells in a co-culture system. In vivo, the combination of anti-PD-1 antibody and cisplatin significantly inhibited tumor growth, while the mechanisms did not involve regulatory T cells. Conclusion: The present data suggested that the blocking of PD-1/PD-L1 axis had a positive prognostic value, which can enhance the chemotherapeutic effect of cisplatin in OS. These findings provide a rationale for utilizing PD1/PD-L1 blocking antibodies as a single agent to cure refractory OS in patients receiving cisplatin treatment. 

Retracted: No

PubPeer comments:
 In this paper, an area of a flow cytometry dot plot has been duplicated and presented as something else. ![file] ,
Tree shrew neural stem cell transplantation promotes functional recovery of tree shrews with a hemi‑sectioned spinal cord injury by upregulating nerve growth factor expression
Authors: Ting-Hua Wang
Piao Zhang
Bin Liu
Yu Shi
Liu-Lin Xiong
Rong-Ping Zhang
Yu Zou
Xie-Jie Dai
Journal: International Journal of Molecular Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: neural stem cells; functional recovery; tree shrews; spinal cord injury; mechanism
Affiliations: Institute of Neurological Disease, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China., Institute of Neuroscience, Animal Zoology Department, Kunming Medical University, Kunming, Yunnan 650031, P.R. China.

Abstract:  The aim of the present study was to determine the effect of implanted neural stem cells (NSCs) on the functional recovery of tree shrews (TSs) subjected to hemi‑sectioned spinal cord injury (hSCI), and to investigate the possible mechanism involved. NSCs (passage 2), derived from the hippocampus of TSs (embryonic day 20), were labeled with Hoechst 33342 and transplanted intraspinally into the hSC of TSs at thoracic level 10 in the acute (immediately after injury) and chronic (day 9 post‑injury) stages. The Basso‑Beattie‑Bresnahan (BBB) score was recorded from days 1 to 16 post‑injury, and the survival, migration, differentiation and neurotrophic factor (NTF) expression in vivo were detected. In vitro and in vivo, the expanded NSCs were able to differentiate into neurons and astrocytes, and secreted a variety of NTFs, including ciliary NTF, transforming growth factor‑β1, glial cell line‑derived NTF, nerve growth factor (NGF), brain‑derived NTF and insulin‑like growth factor. Following transplantation, the BBB score in the TSs with chronic‑stage transplantation exhibited a statistically significant increase, while there was no significant difference in the acute group, compared with the control group. This corresponded with the marked upregulation of NGF indicated by reverse transcription‑quantitative polymerase chain reaction. In conclusion, the transplantation of NSCs into the hSC in the chronic phase, but not the acute stage, of hSCI in non‑human primate TSs is effective and associated with upregulated NGF expression. These findings may provide novel strategies for the treatment of SCI in clinical patients. 

Retracted: No

PubPeer comments:
 Fig. 1A P0 day 5 is part of Fig. 1B tsNSCs 3d of [another paper Hu, et al. 2018] from the same group. I put the two images side-by-side with dimension adjusted to match their scale bars, demonstrating the apparent manipulation of the magnification after cropping a piece of the image to use for a different experiment. ![] ,
The long-term fate of mesenchymal stem cells labeled with magnetic resonance imaging-visible polymersomes in cerebral ischemia
Authors: Jiaji Mao
Yong Wang
Xiang Zhang
Minghui Cao
Bingling Lin
Xintao Shuai
Liejing Lu
Fang Zhang
Jun Shen
Xiaohui Duan
Journal: International Journal of Nanomedicine (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: green fluorescence protein; ischemic stroke; magnetic resonance imaging; mesenchymal stem cells; polymersome
Affiliations: Department of Radiology, Sun Yat-Sen Memorial Hospital., PCFM Lab of Ministry of Education, School of Materials Science and Engineering., BME Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, People's Republic of China.

Abstract:  Understanding the long-term fate and potential mechanisms of mesenchymal stem cells (MSCs) after transplantation is essential for improving functional benefits of stem cell-based stroke treatment. Magnetic resonance imaging (MRI) is considered an attractive and clinically translatable tool for longitudinal tracking of stem cells, but certain controversies have arisen in this regard. In this study, we used SPION-loaded cationic polymersomes to label green fluorescent protein (GFP)-expressing MSCs to determine whether MRI can accurately reflect survival, long-term fate, and potential mechanisms of MSCs in ischemic stroke therapy. Our results showed that MSCs could improve the functional outcome and reduce the infarct volume of stroke in the brain. In vivo MRI can verify the biodistribution and migration of grafted cells when pre-labeled with SPION-loaded polymersome. The dynamic change of low signal volume on MRI can reflect the tendency of cell survival and apoptosis, but may overestimate long-term survival owing to the presence of iron-laden macrophages around cell graft. Only a small fraction of grafted cells survived up to 8 weeks after transplantation. A minority of these surviving cells were differentiated into astrocytes, but not into neurons. MSCs might exert their therapeutic effect via secreting paracrine factors rather than directing cell replacement through differentiation into neuronal and/or glial phenotypes. 

Retracted: No

PubPeer comments:
 Throughout this paper, images seem to have been edited to include repeated regions. One example shows below, from Figure 9A. *** Enhanced brightness ![file] *** Original brightness showing location ![file] , 
 Erratum published October 13, 2021 The authors have advised that Figures 6, 8 and 9 on pages 6713, 6715 and 6716, respectively, of the published paper are incorrect. The errors were introduced by the Editorial staff during the publication process. The correct figures are shown in Download Article. , 
 How can it be that the editorial staff happened to copy parts of micrographs and pasted them on the same image? ,
Prothymosin alpha functions as a cellular oncoprotein by inducing transformation of rodent fibroblasts in vitro
Authors: M A Cotter 2nd
E S Robertson
R S Orre
C Subramanian
Journal: Journal of Biological Chemistry (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Prothymosin alpha; cell proliferation; c-myc; histones; chromatin remodeling
Affiliations: Department of Microbiology and Immunology and Cellular and Molecular Biology Graduate Program, University of Michigan Medical School, Ann Arbor, Michigan 48109-0620, USA.

Abstract:  Prothymosin alpha (ProTalpha), a cellular molecule known to be associated with cell proliferation, is transcriptionally up-regulated on expression of c-myc and interacts with histones in vitro and associates with histone H1 in cells. Previous studies have also shown that ProTalpha is involved in chromatin remodeling. Recent studies have shown that ProTalpha interacts with the acetyl transferase p300 and an essential Epstein-Barr virus protein, EBNA3C, involved in regulation of viral and cellular transcription. These studies suggest a potential involvement in regulation of histone acetylation through the association with these cellular and viral factors. In the current studies, we show that heterologous expression of ProTalpha in the Rat-1 rodent fibroblast cell line results in increased proliferation, loss of contact inhibition, anchorage-independent growth, and decreased serum dependence. These phenotypic changes seen in transfected Rat-1 cells are similar to those observed with a known oncoprotein, Ras, expressed under the control of a heterologous promoter and are characteristic oncogenic growth properties. These results demonstrate that the ProTalpha gene may function as an oncogene when stably expressed in Rat-1 cells and may be an important downstream cellular target for inducers of cellular transformation, which may include Epstein-Barr virus and c-myc. 

Retracted: No

PubPeer comments:
 Figure 3A. Much more similar than expected. https: imgur.com Nn7Nalz , 
 There are three duplications in Figure 3A. Adding the remaining two on top of the one that Cryptocephalus Marginatus found. ![file] , 
 There also seems to be a repeated image in Figure 2. *** ![file] ,
Biotinylated naringenin intensified anticancer effect of gefitinib in urethane-induced lung cancer in rats: favourable modulation of apoptotic regulators and serum metabolomics
Authors: Poonam Parashar
Anupam Guleria
Amit Kumar
Shubhini A Saraf
Jovita Kanoujia
Malti Arya
Chandra Bhushan Tripathi
Abhishek Yadav
Mahendra Singh
Journal: Artificial Cells Nanomedicine and Biotechnology (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: A549 cells; Lung carcinoma; co-therapy; targeted delivery; western blot.
Affiliations: a Department of Pharmaceutical Sciences , Babasaheb Bhimrao Ambedkar University (A Central University) , Lucknow , India., b Centre of Biomedical Research , Lucknow , India.

Abstract:  Co-therapy through biotin modified nanoparticles (NPs) of gefitinib (Gnb) and naringenin (Nar) was investigated for its therapeutic and synergistic potential against lung cancer. The biotin-conjugated polymeric NPs (bty-Nar/Gnb) were developed using oil in water emulsion technique and optimized using central composite design. The formulations were subjected to various in vitro (A549 cell lines) and in vivo evaluations in urethane-induced lung cancer. Co-administration of Gnb and Nar NPs displayed a significant reduction in tumour volume while restoring the biochemical parameters and serum metabolites to normal levels. Significant down-regulation of anti-apoptotic proteins (P-16, MMP-9 and Bcl-2) and up-regulation of pro-apoptotic proteins (caspase-9 and BAX) was displayed with co-therapy. This investigation demonstrated the superiority of co-therapy over individual therapy for improved therapeutic efficacy and is favourable for developing a safe, effective and targeted delivery for lung carcinoma therapy. 

Retracted: No

PubPeer comments:
 Figure: 4 (B) Authors represented a bar diagram of cellular uptake. But there is no clue in the whole research paper that how they quantify it. , 
 Figure 8a appears to have two images which overlap (after change in aspect ratio), but they are described differently. *** ![file] , 
 The images in Figure 2 appear to share the same source, after the aspect ratio is changed. Tellingly, the scale bar and text are distorted in the published 2b. *** ![file] ,
DUOX2 promotes the progression of colorectal cancer cells by regulating the AKT pathway and interacting with RPL3
Authors: Li Feng
Zhenya Zhang
Lianghui Zhi
Xue Zhang
Bin Yu
Lianmei Zhao
Bo Gao
Cong Zhang
Jing Han
Guiying Wang
Da Jiang
Meng Li
Journal: Carcinogenesis (2021)
Discipline: CLINICAL MEDICINE
Keywords: DUOX2; colorectal cancer; invasion; metastasis; prognosis
Affiliations: Department of Medical Oncology, Hebei Medical University Fourth Affiliated Hospital, Shijiazhuang, Hebei, China, The Second General Surgery, Hebei Medical University Fourth Affiliated Hospital, Shijiazhuang, Hebei, China, Scientific Research Center, Hebei Medical University Fourth Affiliated Hospital, Shijiazhuang, Hebei, China, Department of General Surgery, Hebei Medical University Third Affiliated Hospital, Shijiazhuang, Hebei, China

Abstract:  Dual oxidase 2 (DUOX2) is an important regulatory protein in the organic process of thyroid hormone iodine. Mounting evidence suggests that DUOX2 plays a crucial role in the occurrence and development of cancers. However, the function and mechanism of DUOX2 in colorectal cancer (CRC) have not been fully clarified. In the present study, the relationship between the expression of DUOX2 and the clinicopathological features and prognosis of CRC patients was analyzed. Furthermore, the effects of DUOX2 on proliferation and invasion in vitro and in vivo were examined. DUOX2-associated proteins were identified by immunoprecipitation (IP). Next-generation sequencing detection was performed to illustrate the mechanism of DUOX2 in CRC cells. It was found that the expression levels of DUOX2 in metastatic sites were significantly higher than those in primary tumor tissues, and this was demonstrated to be associated with poor prognosis. The knockdown of DUOX2 inhibited the invasion and migration of CRC cells. Furthermore, DUOX2 regulated the stability of ribosomal protein uL3 (RPL3) by affecting the ubiquitination status of RPL3, and the invasion and migration ability of DUOX2 can be reversed by the overexpression of RPL3. The downregulation of DUOX2 can affect the expression level of a large number of genes, and a number of these are enriched in the PI3K-AKT pathway. Some of the changes caused by DUOX2 can be reversed by RPL3. In summary, DUOX2 exhibits a significantly higher expression in CRC tumor samples, and facilitates the invasion and metastasis ability of CRC cells by interacting with RPL3. 

Retracted: No

PubPeer comments:
 1. There are many Akt phosphorylation sites. In this study, which phosphorylation site did the author choose? Please Provide the raw image of p-AKT. 2.The cells seeded on a non M-coated membrane were used for migration assay, and M-coated membrane for invasion assay. From the Fig 4B, it is difficult to tell if Matrigel is covered in invasion assay. ,
miR-429 mediates tumor growth and metastasis in colorectal cancer
Authors: Jie Zhou
Rui Shi
Qian Zhao
Yantao Han
Journal: American journal of cancer research (2017)
Discipline: CLINICAL MEDICINE
Keywords: CRC; HOXA5; MiR-429; metastasis; tumor growth.
Affiliations: Qingdao University Qingdao 266071, Shandong, China., Qingdao University Affiliated Hospital Qingdao 266071, Shandong, China., Qingdao Hiser Medical Center Qingdao 266033, Shandong, China.

Abstract:  Colorectal cancer (CRC), presenting the third most common malignancy worldwide. In recent years, the aberrantly upregulation or downregulation of miRNAs in CRC have been evidenced in a number of studies. In this study, our results showed that the expression of miR-429 was significantly higher in CRC tissue compared with adjacent non-tumor tissue. In addition, our findings showed that miR-429 level was significantly associated with clinicoplathological features and prognosis of patients with CRC. Moreover, our findings showed that miR-429 exerted oncogenic effect by directly targeting HOXA5, a transcription factor of HOX families that is involved in the development and progression of CRC. 

Retracted: Yes

PubPeer comments:
 There is uncertainty whether the corresponding email address belongs to the first author of the present paper, or to Fanbo Jing as in other papers. ![file] Could either author clarify? , 
 Fig 3B.  MiR-429 promotes cell cycle progression and inhibits cell apoptosis.... B. MiR-429 suppresses cell apoptosis, as determined by flow cytometry. Similar or identical images occur frequently within this oeuvre of papers. Below - picking an example at random - Fig 5C from [Gao et al (2017)]  Antitumor effects of hispidulin (20 u00b5M) were abrogated by the ectopic expression of Sphk1 or pretreatment with K6PC-5, an activator of Sphk1. ... C: Effects of hispidulin (20 u00b5M) on the... cell apoptosis... in Caki-2 and A498 cells after overexpressing Sphk1 or pretreatment with Sphk1 activator K6PC-5 ![file] , 
 Below, 2B.  MiR-429 promotes cell proliferation. ... B. MiR-429 promotes long term cell proliferation, as determined by colony formation. Above, Fig 1B from [Li et al (2019)] .  AIF induces apoptosis in CRC cells. ... B. Colony formation assay of HCT-116 and SW480 cells treated with AIF (5 and 10 u00b5M) for the indicated durations. ![file] Surprisingly many colony plates appear in both papers, given that these are different treatments of different cell lines, reported by different authors. , 
 Retracted [1 August 2020] .  A large portion of the data and the text in this article was copied from another source as disclosed by a knowledgeable informant and subsequently confirmed by the Editorial Office. Therefore, the entire article has been retracted in accordance with this journalu2019s policy and editorial decision. ,
Low BRMS1 expression promotes nasopharyngeal carcinoma metastasis in vitro and in vivo and is associated with poor patient survival
Authors: Hui-Yun Wang
Jing Zeng
Lei Chen
Ying Sun
Jing-Ping Yun
Jun Ma
Mo Chen
Ying Guo
Na Liu
Ling-Long Tang
Wen-Fei Li
Bi-Jun Huang
Qing-Mei He
Rui-Xue Cui
Ning Jiang
Journal: BMC Cancer (2012)
Discipline: CLINICAL MEDICINE
Keywords: BRMS1; metastasis; nasopharyngeal carcinoma; prognosis; survival
Affiliations: Department of Radiation Oncology, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China.

Abstract:  Background: Breast cancer metastasis suppressor 1 (BRMS1) is a metastasis suppressor gene. This study aimed to investigate the impact of BRMS1 on metastasis in nasopharyngeal carcinoma (NPC) and to evaluate the prognostic significance of BRMS1 in NPC patients. Methods: BRMS1 expression was examined in NPC cell lines using quantitative reverse transcription-polymerase chain reaction and Western blotting. NPC cells stably expressing BRMS1 were used to perform wound healing and invasion assays in vitro and a murine xenograft assay in vivo. Immunohistochemical staining was performed in 274 paraffin-embedded NPC specimens divided into a training set (n = 120) and a testing set (n = 154). Results: BRMS1 expression was down-regulated in NPC cell lines. Overexpression of BRMS1 significantly reversed the metastatic phenotype of NPC cells in vitro and in vivo. Importantly, low BRMS1 expression was associated with poor distant metastasis-free survival (DMFS, P &lt; 0.001) and poor overall survival (OS, P &lt; 0.001) in the training set; these results were validated in the testing set and overall patient population. Cox regression analysis demonstrated that low BRMS1 expression was an independent prognostic factor for DMFS and OS in NPC. Conclusions: Low expression of the metastasis suppressor BRMS1 may be an independent prognostic factor for poor prognosis in NPC patients. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. , 
 #1 I agree with the concern posted above, and also note that Figure 2A appears to have 2 images which overlap, after horizontal stretch. Difficult to see how this could occur merely due to an error during figure assembly. *** ![file] ,
Critical interactions between TGF-beta signaling/ELF, and E-cadherin/beta-catenin mediated tumor suppression
Authors: B Mishra
A N Sidawy
L Mishra
E P Reddy
S Evans
C Li
Y Tang
C-X Deng
V Katuri
W Jogunoori
A Rashid
Journal: Oncogene (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TGF-beta pathway; gastrointestinal tumors; ELF; Smad4; E-cadherin
Affiliations: Laboratory of Cancer Genetics, Digestive Diseases, and Developmental Molecular Biology, Department of Surgery, Medicine, Lombardi Cancer Center, Georgetown University, Washington, DC, USA., Fels Institute for Cancer Research and Molecular Biology, Temple University, Philadelphia, PA, USA., Genetics of Development and Disease Branch, NIDDK, NIH, Bethesda, MD, USA., Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA., Department of Surgery, Washington, DC, USA., Department of Veterans Affairs, Washington, DC, USA.

Abstract:  Inactivation of the transforming growth factor-beta (TGF-beta) pathway occurs often in malignancies of the gastrointestinal (GI) system. However, only a fraction of sporadic GI tumors exhibit inactivating mutations in early stages of cancer formation, suggesting that other mechanisms play a critical role in the inactivation of this pathway. Here, we show a wide range of GI tumors, including those of the stomach, liver and colon in elf+/- and elf+/- / Smad4+/- mutant mice. We found that embryonic liver fodrin (ELF), a beta-Spectrin originally identified in endodermal stem/progenitor cells committed to foregut lineage, possesses potent antioncogenic activity and is frequently inactivated in GI cancers. Specifically, E-cadherin accumulation at cell-cell contacts and E-cadherin-beta-catenin-dependent epithelial cell-cell adhesion is disrupted in elf+/- / Smad4+/- mutant gastric epithelial cells, and could be rescued by ectopic expression of full-length elf, but not Smad3 or Smad4. Subcellular fractionation revealed that E-cadherin is expressed mainly at the cell membrane after TGF-beta stimulation. In contrast, elf+/- / Smad4+/- mutant tissues showed abnormal distribution of E-cadherin that could be rescued by overexpression of ELF but not Smad3 or Smad4. Our results identify a group of common lethal malignancies in which inactivation of TGF-beta signaling, which is essential for tumor suppression, is disrupted by inactivation of the ELF adaptor protein. 

Retracted: No

PubPeer comments:
 Dublicated FACS blots in Fig 3: ![file] Apart from that, how could Western blots be quantified? Blots are heavily overloaded and exposure is far from beeing linear, e.g. Fig 5: ![file] ,
Vimentin participates in microglia activation and neurotoxicity in cerebral ischemia
Authors: Amy Aylsworth
Sheng T Hou
Jacqueline Slinn
Susan X Jiang
Journal: Journal of Neurochemistry (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Microglia; activation; neurotoxicity; vimentin; neurodegenerative diseases
Affiliations: Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada.

Abstract:  Microglia are the 'immune cells' of the brain and their activation plays a vital role in the pathogenesis of many neurodegenerative diseases. Activated microglia produce high levels of pro-inflammatory factors, such as TNFα, causing neurotoxicity. Here we show that vimentin played a key role in controlling microglia activation and neurotoxicity during cerebral ischemia. Deletion of vimentin expression significantly impaired microglia activation in response to LPS in vitro and transient focal cerebral ischemia in vivo. Reintroduction of the functional vimentin gene back into vimentin knockout microglia restored their response to LPS. More importantly, impairment of microglia activation significantly protected brain from cerebral ischemia-induced neurotoxicity. Collectively, we demonstrate a previously unknown function of vimentin in controlling microglia activation. 

Retracted: No

PubPeer comments:
 Fig 5b, the top left panel and the bottom right panel appears to partially overlap, but they refer to different mice (VIM+ + vs VIM- -) and anatomical location (contralateral vs ipsilateral). ![file] , 
 Images in Figure 1 and 2 appear to overlap (cyan boxes), but seem to be described differently. Could the authors please check? u201cThis research is supported by the Heart and Stroke Foundation of Ontario grant (Number T5760, T6706) and Canadian Institutes of Health Research grant (Number CCI85680) to STH.u201d *** ![file] ,
HuR promotes miRNA-mediated upregulation of NFI-A protein expression in MDSCs during murine sepsis
Authors: Mohamed El Gazzar
Charles E McCall
Dima Youssef
Tuqa Alkhateeb
Gregory A Hawkin
Ajinkya Kumbhare
Isatou Bah
Zhi Q Yao
Journal: Molecular Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: MDSC; NFI-A; Sepsis; miRNA.
Affiliations: Department of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA., Department of Biochemistry and Center for Precision Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA., Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, 27157, USA., Department of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN, 37614, USA. Electronic address: .

Abstract:  Myeloid-derived suppressor cells (MDSCs) contribute to high mortality rates during sepsis, but how sepsis induces MDSCs is unclear. Previously we reported that microRNA (miR)-21 and miR-181b reprogram MDSCs in septic mice by increasing levels of DNA binding transcription factor, nuclear factor 1 (NFI-A). Here, we provide evidence that miR-21 and miR-181b stabilize NFI-A mRNA and increase NFI-A protein levels by recruiting RNA-binding proteins HuR and Ago1 to its 3' untranslated region (3'UTR). We also find that the NFI-A GU-rich element (GRE)-binding protein CUGBP1 counters miR-21 and miR-181b dependent NFI-A mRNA stabilization and decreases protein production by replacing 3'UTR bound Ago1 with Ago2. We confirmed the miR-21 and miR-181b dependent reprogramming pathway in MDSCs transfected with a luciferase reporter construct containing an NFI-A 3'UTR fragment with point mutations in the miRNA binding sites. These results suggest that targeting NFI-A in MDSCs during sepsis may enhance resistance to uncontrolled infection. 

Retracted: No

PubPeer comments:
 Image duplication. ![file] , 
 The authors regret that the upper protein bands (NFI-A) in Fig. 6C is a duplicate of the lower band (actin) in Fig. 3E. This was due to a mistake in the cutting and alignment of the correct bands. We have restored the correct bands in Figure 6C. This correction does not influence the results or the study s conclusions. The authors would like to apologize for any inconvenience caused. ![file] ,
RETRACTED ARTICLE: The biological function of long noncoding RNA FAL1 in oesophageal carcinoma cells
Authors: Fang Liu
Cuiping Liu
Zhiguo Yang
Dan Wu
Dongyan Liu
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: FAL1; Long non-coding RNAs; cell proliferation; oesophageal squamous cell carcinoma.
Affiliations: a Department of Oncology , Heze municipal hospital , Heze , Shandong , China.

Abstract:  Long non-coding RNAs (lncRNAs) have been reported to be involved in the pathogenesis of a variety of malignancies, including oesophageal cancer. Alterations of the lncRNA focally amplified lncRNA on chromosome 1 (FAL1) are present in epithelial tumours. However, its expression pattern and function in oesophageal cancer are poorly addressed. In the current study, we reported that FAL1 is upregulated in oesophageal cancer tissues and is positively correlated with outcomes in oesophageal squamous cell carcinoma (OSCC). Consecutive experiments revealed that the expression level of FAL1 is higher in OSCC cell lines than in human normal oesophageal epithelium cell line HEEpiCs. Importantly, Knockdown of FAL1 suppressed cell proliferation, increased cell cycle arrest, inhibited cell invasion and epithelial-mesenchymal transition (EMT) by affected related genes. In contrast, overexpression of FAL1 has the opposite effects. Our findings underline a novel biological mechanism in which FAL1 acts as a regulator of oesophageal cancer cells and may provide insights into novel therapeutic strategies for oesophageal cancer. 

Retracted: Yes

PubPeer comments:
 Figure 2C. Much more similar than expected. ![file] ,
CD133(+) single cell-derived progenies of colorectal cancer cell line SW480 with different invasive and metastatic potential
Authors: Xiaoqin Xiao
Yanqing Ding
Yongjian Deng
Jian Yuan
Guangqiu Li
Junmei Hao
Chao Liu
Na Tang
Xiuwu Bian
Hongwei Wang
Journal: Clinical & Experimental Metastasis (2010)
Discipline: CLINICAL MEDICINE
Keywords: Single cell progenies; cancer initiating cell; CD133; colorectal cancer stem cells; metastatic cancer stem cells
Affiliations: Department of Pathology, Southern Medical University, Guangzhou, People's Republic of China.

Abstract:  Single cell progenies (SCPs) inherit biological properties from their isogenetic mother cells. If a single cancer cell can give rise to progenies, which can be passaged sustainably in vitro and produce tumor in xenotransplantation, the cell should be cancer initiating cell. CD133 (Prominin-1, Prom1) is the marker of human colorectal cancer (CRC) stem cells and probably a marker of metastatic cancer stem cells (CSCs). Thirty-three SCPs of CRC cell line SW480 were isolated by limited dilution methods, thirty of which are CD133 positive and three negative. All of the CD133(+) SCPs are tumorigenic, and the subcutaneous tumors expanded rapidly, while only 1 of 3 CD133(-) SCPs developed a minimal tumor in nude mice. Orthotopic transplantation experiments showed that CD133(+) SCPs possessed heterogeneity in intestinal wall invasion, lymph node and liver metastases. CD133(+) SCPs varied in cell growth, invasive ability, epithelial-mesenchymal-transition and expression of CSCs markers (CD133, CD44, and CXCR4) associated with metastatic potential. CD133(-) SCPs did not produce secondary transplanted tumor, intestinal invasion and metastasis. The results indicated CD133(+) subpopulation of SW480 SCPs bear heterogeneous invasive and metastatic ability, and CRC-CSCs might be a heterogeous subpopulation. 

Retracted: No

PubPeer comments:
 There seem to be unexpectedly repeated elements in one image of Figure 2. *** ![file] *** ![file] , 
 There seem to be 2 sets of unexpectedly similar plots in Figure 6D. *** ![file] ,