PReD-Bench/PRed-Bench huggingface dataset:
A water-soluble polysaccharide from the roots of Polygala tenuifolia suppresses ovarian tumor growth and angiogenesis in vivo
Authors: Dan Xu
Hua Yao
Yunduo Liu
Fubin Zhang
Qinghua Tian
Ping Cui
Journal: International Journal of Biological Macromolecules (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Antiangiogenesis; Human ovarian cancer; Polygala tenuifolia; Polysaccharide; Vascular endothelial growth factor.
Affiliations: Department of Medical Oncology, Harbin Chest Hospital, Harbin 150001, China., Department of Gynecological Oncology, Harbin Medical University Cancer Hospital, Harbin 150040, China., Department of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China., Department of Intensive Care Unit, Chinese PLA 211 General Hospital, Harbin 150080, China., Department of Gynecological Oncology, Harbin Medical University Cancer Hospital, Harbin 150040, China. Electronic address: .

Abstract:  PTP, one polysaccharide extracted from the roots of Polygala tenuifolia, has displayed anti-cancer activity in several types of ovarian cancer cells. This study aims to elucidate the structure of PTP and investigate its anticancer effects against SKOV3 xenograft tumor growth in BALB/c mice, as well as the underlying mechanisms involved. GC-MS and NMR data indicate that PTP has a backbone composed of 1,4,6-linked-Œ≤-Galp, 1,4-linked-Œ≤-Galp and 1,4-linked-Œ≤-Glcp, with non-reducing terminal 1-linked-Œ±-Glcp attached to O-6 of 1,4,6-linked-Œ≤-Galp. The tumor growth was suppressed in mice following two week's PTP administration (10, 20 and 40mg/kg) due to the induction of apoptosis, as detected by TUNEL assay. Moreover, lower serum VEGF and EGFR levels were observed in BALB/c mice treated with different doses of PTP when compared with that in untreated mice. Also, EGFR, VEGF, and CD34 were decreased in both transcript and protein levels in the tumor-bearing mice upon PTP treatment. Taken together, our data suggest that PTP appears to be a powerful chemopreventive agent for the patients with ovarian cancer, especially at advanced stage. 

Retracted: No

PubPeer comments:
  Fig. 1. Apoptosis detected using TUNEL assay in BALB c mice treated with (A) PBS (negative control group); (B) PTP (10 mg kg); (C) PTP (20 mg kg); and (D) PTP (40 mg kg). (E) The apoptosis index in BALB c mice treated with different doses of PTP (10, 20 and 40 mg kg). (B) and (D) appear to be overlapping sections of a single larger image.  ,
Astaxanthin Inhibits Expression of Retinal Oxidative Stress and Inflammatory Mediators in Streptozotocin-Induced Diabetic Rats
Authors: Chang-Hao Yang
Wei-Shiung Yang
Po-Ting Yeh
Chung-May Yang
Hsin-Wei Huang
Journal: PLoS ONE (2016)
Discipline: Multidisciplinary
Keywords: astaxanthin; oxidative damage; ocular tissues; streptozotocin; diabetic rats
Affiliations: Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan., Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan., Department of Ophthalmology, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan., Department of Ophthalmology, College of Medicine, National Taiwan University, Taipei, Taiwan., Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan., Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.

Abstract:  Purpose: We evaluated whether orally administered astaxanthin (AST) protects against oxidative damage in the ocular tissues of streptozotocin (STZ)-induced diabetic rats. Methods and results: Fifty 6-week-old female Wistar rats were randomly assigned to receive an injection of STZ to induce diabetes (n = 40) or to remain uninduced (n = 10). The diabetic rats were randomly selected into four groups and they were separately administered normal saline, 0.6 mg/kg AST, 3 mg/kg AST, or 0.5 mg/kg lutein daily for eight weeks. Retinal functions of each group were evaluated by electroretinography. The expression of oxidative stress and inflammatory mediators in the ocular tissues was then assessed by immunohistochemistry, western blot analysis, ELISA, RT-PCR, and electrophoretic mobility shift assay (EMSA). Retinal functions were preserved by AST and lutein in different levels. Ocular tissues from AST- and lutein-treated rats had significantly reduced levels of oxidative stress mediators (8-hydroxy-2'-deoxyguanosine, nitrotyrosine, and acrolein) and inflammatory mediators (intercellular adhesion molecule-1, monocyte chemoattractant protein-1, and fractalkine), increased levels of antioxidant enzymes (heme oxygenase-1 and peroxiredoxin), and reduced activity of the transcription factor nuclear factor-kappaB (NF-Œ∫B). Conclusion: The xanthophyll carotenoids AST and lutein have neuroprotective effects and reduce ocular oxidative stress, and inflammation in the STZ diabetic rat model, which may be mediated by downregulation of NF-Œ∫B activity. 

Retracted: No

PubPeer comments:
 Figures 4 and 5: * Red boxes: Three lanes in the GAPDH panel of Figure 4D look similar to the GAPDH panel in Figure 5D.   The present study was supported by the Natural Science Foundation of Gansu Province (no. 1606RJZA348) and the Science and Technology Project of Lanzhou city (2015-2-67). ,
Salt, blood pressure and cardiovascular risk: what is the most adequate preventive strategy? A Swiss perspective
Authors: Gregoire Wuerzner
Murielle Bochud
Michel Burnier
Journal: Frontiers in Physiology (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: blood pressure; cardiovascular risk; health strategies; hypertension; potassium
Affiliations: Service of Nephrology and Hypertension, Department of Medicine, University Hospital Lausanne, Switzerland., Institut Universitaire de M√©decine Sociale et Pr√©ventive, University Hospital Lausanne, Switzerland.

Abstract:  Among the various strategies to reduce the incidence of non-communicable diseases reduction of sodium intake in the general population has been recognized as one of the most cost-effective means because of its potential impact on the development of hypertension and cardiovascular diseases. Yet, this strategic health recommendation of the WHO and many other international organizations is far from being universally accepted. Indeed, there are still several unresolved scientific and epidemiological questions that maintain an ongoing debate. Thus what is the adequate low level of sodium intake to recommend to the general population and whether national strategies should be oriented to the overall population or only to higher risk fractions of the population such as salt-sensitive patients are still discussed. In this paper, we shall review the recent results of the literature regarding salt, blood pressure and cardiovascular risk and we present the recommendations recently proposed by a group of experts of Switzerland. The propositions of the participating medical societies are to encourage national health authorities to continue their discussion with the food industry in order to reduce the sodium intake of food products with a target of mean salt intake of 5-6 grams per day in the population. Moreover, all initiatives to increase the information on the effect of salt on health and on the salt content of food are supported. 

Retracted: No

PubPeer comments:
 Burnier et al cite a 2008 paper by Paterna et al published in Clinical Science that has shown to contain data duplicated in a later study from the same author group published in the Journal of Cardiac Failure (Parinnello 2009). Data from both these studies were contained in a 2012 systematic review published in BMJ Heart journal that was later retracted (Aug 21, 2012) due to the inability of the study group to provide the original data to verify the duplicate data issues due to a u201ccomputer failureu201d. u2028Additional PubPeer posts for the specific studies are available: https: pubpeer.com publications E03BB72DBAA939C61082F4608D558B https: pubpeer.com publications B24491C479E0C003418D1F1CBECE07 A complete blog of the story leading to retraction of the BMJ Heart systematic review is available here: https: www.cebm.net 2019 02 salt-reduction-in-heart-failure-where-has-the-uncertainty-come-from ,
Thiol-modified chitosan sulfate nanoparticles for protection and release of basic fibroblast growth factor
Authors: Shu-Huei Yu
Yi-Cheng Ho
Shao-Jung Wu
Fwu-Long Mi
Hsing-Wen Sung
Ya-Lin Chiu
Nilendu Panda
Journal: Bioconjugate Chemistry (2010)
Discipline: CHEMISTRY
Keywords: Chitosan derivatives; 6-O-carboxymethylchitosan; Sulfated; Basic fibroblast growth factor; Thiol modification
Affiliations: Department of Biotechnology, Nano Materials R&D Center, and Department of Polymer Materials, Vanung University, Chung-Li, Taiwan, ROC, Department of Chemical Engineering, MingChi University of Technology, Taipei, Taiwan, ROC, and Department of Chemical Engineering, National Tsing Hua University, Hsinchu, Taiwan, ROC

Abstract:  A series of chitosan (CS) derivatives, the 6-O-carboxymethylchitosan (6-O-CC), 2-N sulfated 6-O-carboxymethylchitosan (N-SOCC) and the 2-N and 3,6-O sulfated 6-O-carboxymethyl chitosan (N,O-SOCC) were synthesized in this study. The chemical structures and the degrees of substituted carboxymethyl and sulfate groups of the synthesized compounds were respectively determined by FT-IR spectra and elemental analysis. N,O-SOCC displayed the highest protective efficiency for basic fibroblast growth factor (bFGF) as examined by the L929 fibroblast culture test and docking simulation. N,O-SOCC-4-thio-butylamidine (TBA) conjugates prepared by modification of N,O-SOCC with 2-iminothiolane were in situ cross-linkable. The degrees of thiol substitution of the 2-iminothiolane modified N,O-SOCC polymers were determined to be in the ranges of 45.9 +/- 3.7 and 415.6 +/- 12.5 micromol SH/g SOCC by quantifying the amount of thiol groups on the thiolated polymers with Ellman's reagent. The 2-iminothiolane modified N,O-SOCC and CS complex could be used for preparing nanoparticles by a polyelectrolyte self-assembly method, and the release of bFGF from the nanoparticles was successfully controlled. L929 fibroblast culture tests showed that the thiol modified N,O-SOCC/CS nanoparticles could effectively protect bFGF from inactivation over a 120 h period. The results of this study suggest that the thiol modified N,O-SOCC/CS nanoparticles may be useful as novel materials for specific delivery of bFGF with mitogenic activity. 

Retracted: No

PubPeer comments:
  Could the authors comment on the fact that the noise of these 2 NMR spectra look similar (Figure 2)? ,
MiR-296-5p inhibits cell invasion and migration of esophageal squamous cell carcinoma by downregulating STAT3 signaling
Authors: Y-R Luo
Z-Z Wang
Y-J Cui
X-F Jin
J Du
X-Z Yang
Y Yu
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-296-5p; STAT3; ESCC; tumorigenesis; cell migration
Affiliations: Department of Thoracic Surgery, Affiliated Hospital of Qingdao University, Qingdao, China. .

Abstract:  Objective: Many studies have emphasized the function of microRNA-296 (miR-296) that inhibits tumor formation. To some extent, the role of miR-296 in esophageal squamous cell carcinoma (ESCC) remains misleading. Therefore, the current research was designed to investigate the regulatory mechanisms of miR-296 and signal transducer and activator of transcription 3 (STAT3) in ESCC. Patients and methods: The mRNA expression of miR-296-5p and STAT3 in ESCC tissues or cell lines was measured via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The protein level of STAT3 was measured by Western blotting assay. The Luciferase reporter assay was used to verify the binding sites between miR-296-5p and STAT3. The transwell assay was employed to identify cell migration and invasion. Results: Down-regulation of miR-296-5p was detected in ESCC tissues and cell lines (p&lt;0.01). Additionally, miR-296-5p was found to target STAT3 directly. Functionally, up-regulation of miR-296-5p or down-regulation of STAT3 significantly inhibited cell migration and invasion in ESCC. Conclusions: MiR-296-5p inhibited cell invasion and migration in ESCC by downregulating STAT3. The overexpression of miR-296-5p by targeting STAT3 suppressed tumorigenesis of ESCC cells. 

Retracted: No

PubPeer comments:
 Could the authors please clarify the difference between Figure 1A and Figure 1B? They appear to be showing the same experiment, i.e RT-PCR detection of miR-296-5p expression in normal vs. tumor tissues, but the results shown are different.  , 
 Figures 2B, 4C, and 5C. Some cells or groups of cells appear to be visible multiple times. I have marked some of those with boxes of the same color and shape, without trying to be comprehensive.    ,
TLR4-mediated hippocampal MMP/TIMP imbalance contributes to the aggravation of perioperative neurocognitive disorder in db/db mice
Authors: Xiahao Ding
Jiaxin Li
Bo Gui
Yahe Ge
Hailin Liu
Hongquan Dong
Cunming Liu
Yang Zhang
Zixuan Chen
Nana Li
Tengfei Ma
Min Yu
Journal: Neurochemistry international (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Blood-brain barrier; Db/db mice; Matrix metalloproteinase; Perioperative neurocognitive disorders; Tissue inhibitors of matrix metalloproteinase
Affiliations: Department of Anesthesiology and Perioperative Medicine, 1st Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, China., Department of Anesthesiology, Huai'an First People's Hospital, Huai'an, Jiangsu, 223300, China., Institute for Stem Cell and Neural Regeneration, School of Pharmacy, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, China., Department of Anesthesiology and Perioperative Medicine, 1st Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210029, China. Electronic address: .

Abstract:  Although type 2 diabetes is an important predictor of perioperative neurocognitive disorder (PND), little is currently known about its mechanism of action. Adult male db/db and db/m mice were subjected to four different treatments, including either sham or tibial fracture surgery as well as intraperitoneal injection of vehicle or TAK-242 (the selective inhibitor of TLR4) at 1, 24, and 48 h after surgery. The fear conditioning test was performed to detect cognitive impairment on post-operative day (POD) 3. The hippocampus was collected on POD 1 for western-blots and on POD 3 for western-blots, transmission electron microscopy, and electrophysiological experiments. Toll-like receptor 4 (TLR4) inhibition reversed more profound decline in the freezing behavior of db/db mice on POD 3. The surgery reduced the slope of hippocampal field excitatory postsynaptic potentials, and induced blood-brain barrier (BBB) damage in db/db mice on POD 3. The surgery also increased protein levels of TLR4, tumor necrosis factor (TNF)-Œ±, interleukin (IL)-1Œ≤, albumin, matrix metalloproteinase (MMP)-2, and MMP-9, and decreased protein levels of claudin-5, occludin, tissue inhibitor of matrix metalloproteinase (TIMP)-1, and TIMP-2 in the hippocampus of db/db and db/m mice. These changes were all reversed by TAK-242 treatment. At last, compared with those in post-operative db/m mice, the surgery increased protein levels of TLR4, TNF-Œ±, and IL-1Œ≤, decreased protein levels of claudin-5 and occludin, and sustained the MMP/TIMP imbalance in the hippocampus of db/db mice on POD 3. Our results suggest that TLR4-mediated aggravated hippocampal MMP/TIMP imbalance, BBB disruption, sustained inflammatory cytokine release, and impairment of long-term potentiation play a key role in tibial fracture surgery-induced persistent PND in db/db mice. 

Retracted: No

PubPeer comments:
 Could the authors explain why similar bands shown in two different papers?  ,
n-3 Fatty Acids Induce Neurogenesis of Predominantly POMC-Expressing Cells in the Hypothalamus
Authors: Gabriela F P Souza
L√≠cio A Velloso
Joseane Morari
Hernandes F Carvalho
Carina Solon
Rodrigo F Moura
Lucas F R Nascimento
Guilherme O Barbosa
Daniela S Razolli
Let√≠cia M Ign√°cio-Souza
Sheila C Vict√≥rio
Journal: Diabetes (2016)
Discipline: CLINICAL MEDICINE
Keywords: Apoptosis; hypothalamic neurons; obesity; neurogenesis; n-3 polyunsaturated fatty acids (PUFAs)
Affiliations: Laboratory of Cell Signaling, University of Campinas, Campinas, Brazil., Department of Cell Biology, University of Campinas, Campinas, Brazil., Laboratory of Cell Signaling, University of Campinas, Campinas, Brazil .

Abstract:  Apoptosis of hypothalamic neurons is believed to play an important role in the development and perpetuation of obesity. Similar to the hippocampus, the hypothalamus presents constitutive and stimulated neurogenesis, suggesting that obesity-associated hypothalamic dysfunction can be repaired. Here, we explored the hypothesis that n-3 polyunsaturated fatty acids (PUFAs) induce hypothalamic neurogenesis. Both in the diet and injected directly into the hypothalamus, PUFAs were capable of increasing hypothalamic neurogenesis to levels similar or superior to the effect of brain-derived neurotrophic factor (BDNF). Most of the neurogenic activity induced by PUFAs resulted in increased numbers of proopiomelanocortin but not NPY neurons and was accompanied by increased expression of BDNF and G-protein-coupled receptor 40 (GPR40). The inhibition of GPR40 was capable of reducing the neurogenic effect of a PUFA, while the inhibition of BDNF resulted in the reduction of global hypothalamic cell. Thus, PUFAs emerge as a potential dietary approach to correct obesity-associated hypothalamic neuronal loss. 

Retracted: No

PubPeer comments:
 **Figure 2.** Red square in panel G is the ventromedial nucleus, not the paraventricular nucleus. This is a very serious concern if measurements were made in this region in the rest of the work. **Figure 3.** Panel D. DHA treatment seems manipulated to show positive yellow cells, as ventricle walls shows an evident change of color (from blue to purple):   ,
TCRP1 promotes radioresistance of oral squamous cell carcinoma cells via Akt signal pathway
Authors: Yixue Gu
Zhimin He
Binjie Liu
Yongmei Ouyang
Shasha Fan
Guopei Zheng
Yanhui Yu
Journal: Molecular and Cellular Biochemistry (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Tongue cancer resistance-associated protein 1 (TCRP1); chemotherapeutic resistance; radioresistance; oral squamous cell carcinoma (OSCC); Tca8113/TCRP1
Affiliations: Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, Hunan, China.

Abstract:  Tongue cancer resistance-associated protein 1 (TCRP1) is a novel gene located on human chromosome 11q13.4 which has been reported as a candidate related to chemotherapeutic resistance to cisplatin. Results suggest that TCRP also contribute to radioresistance in oral squamous cell carcinoma (OSCC) cells. We previously established exogenous overexpression of TCRP1 cell line Tca8113/TCRP1 and TCRP1 knockdown cell line Tca8113/PYM-siRNA and paired control cell lines, which provides a cell model system to investigate the roles and mechanisms of TCRP1-mediated radioresponse in OSCC. In this study, we first compared the radiosensitivity of up/down-regulating expression of TCRP1 cell lines and paired control cell lines by a clonogenic survival assay, Hoechst 33258 staining, cell growth assay, and comet assay. The results indicated that TCRP1 played a significant role in mediating OSCC radioresistance through decreased cells apoptosis and increased cellular proliferation and long-term survival. The further study found that TCRP1 function by up-regulating Akt activity and levels and then elevating the level of NF-Œ∫B. In summary, these results provided strong evidence for the linkage between TCRP1 and radiation sensitivity and may provide theoretical base of TCRP1 as a potential molecular mark of estimating the response for irradiation in OSCC. 

Retracted: No

PubPeer comments:
 Figure 2. * Blue boxes: Two panels in the 48h post-IR row appear to show an overlap.  , 
 Figure 1A and 3C: * Red boxes: the alpha-Tublin (sic) panels appear to look very similar, but the samples are shown in a different order.  Reported to the journal in October 2015, with a reminder in 2017, but no outcome yet. ,
Nell‚Ä?‚ÄêŒîE, a novel transcript of Nell‚Ä?, inhibits cell migration by interacting with enolase‚Ä?
Authors: Qian Zhang
Xueyan Qin
Kang Ting
Feng Chen
Jiuxiang Lin
Huaxiang Zhao
Xinli Zhang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: alpha-enolase; cell migration assays; isoforms; nel-like protein 1; protein-protein interaction
Affiliations: Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, P. R. China., Central Laboratory, Peking University School and Hospital of Stomatology, Beijing, P. R. China., Dental and Craniofacial Research Institute, University of California, Los Angeles, California.

Abstract:  NELL-1 is a secreted protein that was originally found to be upregulated in pathologically fusing and fused sutures in non-syndromic unilateral coronal synostosis patients. Apart from the ability of NELL-1 to promote osteogenesis in long and craniofacial bones, NELL-1 reportedly inhibits the formation of several benign and malignant tumors. We previously identified a novel transcript of Nell-1 that lacked a calcium-binding epidermal growth factor (EGF)-like domain compared with full-length Nell-1; this new transcript was named Nell-1-ŒîE. Three obvious structural differences between these two isoforms were revealed by homology modeling. Furthermore, the recombinant Nell-1-ŒîE protein, but not the full-length Nell-1 protein, inhibited cell migration in vitro. However, full-length Nell-1 and Nell-1-ŒîE proteins were present in similar subcellular locations and displayed similar expression patterns in both the intracellular and extracellular spaces. The results from the co-immunoprecipitation and liquid chromatography/tandem mass spectrometry analyses using two cell lines demonstrated that Nell-1-ŒîE but not full-length Nell-1 interacted with enolase-1 in the extracellular spaces of both cell lines. The results of wound healing assays using ENO-1-overexpressing cells treated with full-length Nell-1/Nell-1-ŒîE suggested that Nell-1-ŒîE inhibited cell migration by interacting with ENO-1. Our study indicated that the novel transcript Nell-1-ŒîE, but not full-length Nell-1, might be a candidate tumor suppressor factor for basic research and clinical practice. 

Retracted: No

PubPeer comments:
 When publishing an erratum, the publisher should have done something with the poor quality Western immuno blots in Figure 3 and 4. It is impossible to judge the data.   ,
Down-regulation of XIAP enhances the radiosensitivity of esophageal cancer cells in vivo and in vitro
Authors: Dong-Mei Wu
Gao Yi
Xin-Rui Han
Xin Wen
Lu Chen
Jun Lu
Shao-Hua Fan
Zi-Feng Zhang
Yuan-Lin Zheng
Journal: Bioscience Reports (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Esophageal cancer; Gene silencing; Radiosensitivity; Viability; XIAP
Affiliations: Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China., Department of Oncology, Linyi Cancer Hospital, Linyi 276000, P.R. China., Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, P.R. China   .

Abstract:  The study investigated the effects of X-chromosome-linked inhibitor of apoptosis (XIAP) gene silencing on the radiosensitivity of esophageal cancer (EC) cells. Western blotting was used to select EC cell lines with XIAP overexpression. Selected EC9706 and KYSE30 cell lines were both divided into four groups: the blank control group, the negative control (NC) group (transfected with pBSHH1), the siRNA-enhanced group (transfected with pBSHH1-XIAP1-siRNA), and the siRNA-decreased group (transfected with pBSHH1-XIAP2-siRNA). Expressions of XIAP were measured by reverse-transcription quantitative PCR (RT-qPCR) and Western blotting, cell survival and viability by MTT assay and colony formation assay, and cell apoptosis by flow cytometry, respectively. Caspase-3 and caspase-9 activity were detected using caspase-3 and caspase-9 activity detection kits. A nude mice model of EC9706 cell line was established to measure tumorigenesis ability. Compared with the NC group, XIAP mRNA and protein expressions were decreased, caspase-3 and caspase-9 activity and apoptosis were up-regulated, and cell survival rate and colony-forming efficiency were lower in the siRNA-enhanced and siRNA-decreased groups in both the cell lines; while the opposite trends were found in the siRNA-decreased group compared with the siRNA-enhanced group. Tumor weight and volume of nude mice were decreased in the siRNA-enhanced and siRNA-decreased groups than those in the NC group, and were elevated in the siRNA-decreased group compared with the siRNA-enhanced group. These results indicate that XIAP gene silencing would strengthen the radiosensitivity of EC9706 cells, which provides a novel target for the treatment of EC. 

Retracted: No

PubPeer comments:
 Figure 5A appears to have two images which overlap. ***  ,
Oncogenic Ras and B-Raf proteins positively regulate death receptor 5 expression through co-activation of ERK and JNK signaling
Authors: Wei Zhou
Ping Yue
Shi-Yong Sun
You-Take Oh
Esther P Black
Taofeek K Owonikoko
Justin M Balko
Fadlo R Khuri
Journal: Journal of Biological Chemistry (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Oncogenic mutations; Ras; B-Raf; DR5; apoptosis
Affiliations: Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, Georgia 30322, USA.

Abstract:  Oncogenic mutations of ras and B-raf frequently occur in many cancer types and are critical for cell transformation and tumorigenesis. Death receptor 5 (DR5) is a cell surface pro-apoptotic death receptor for tumor necrosis factor-related apoptosis-inducing ligand and has been targeted in cancer therapy. The current study has demonstrated induction of DR5 expression by the oncogenic proteins Ras and B-Raf and revealed the underlying mechanisms. We demonstrated that both Ras and B-Raf induce DR5 expression by enforced expression of oncogenic Ras (e.g. H-Ras12V or K-Ras12V) or B-Raf (i.e. V600E) in cells and by analyzing gene expression array data generated from cancer cell lines and from human cancer tissues. This finding is further supported by our results that knockdown of endogenous K-Ras or B-Raf (V600E) reduced the expression of DR5. Importantly, we have elucidated that Ras induces DR5 expression through co-activation of ERK/RSK and JNK signaling pathways and subsequent cooperative effects among the transcriptional factors CHOP, Elk1, and c-Jun to enhance DR5 gene transcription. Moreover, we found that the majority of cancer cell lines highly sensitive to the DR5 agonistic antibody AMG655 have either Ras or B-Raf mutations. Our findings warrant further study on the biology of DR5 regulation by Ras and B-Raf, which may provide new insight into the biology of Ras and B-Raf, and on the potential impact of Ras or B-Raf mutations on the outcome of DR5-targeted cancer therapy. 

Retracted: No

PubPeer comments:
 Figure 2C. Much more similar than you would expect. https: imgur.com Y5yT0TT , 
 Thanks for your hard work and meticulous examination. We checked our original data as shown in the attached file, which shows tubulin for each cell line. This should be an error introduced during the preparation of the figure. Sorry for this confusion.  , 
 2020 correction. https: www.jbc.org content 295 26 8870.short During preparation of Fig. 2C, the actin control for BCPAP cells was inadvertently used for LOXIMVI. This error has now been corrected and does not affect the results or conclusions of this work. ,
Small RNA analysis in Sindbis virus infected human HEK293 cells
Authors: Irina Mohorianu
Andras Donaszi-Ivanov
Tamas Dalmay
Penny P Powell
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: RNA interference; virus infection; alphavirus; Sindbis virus; HEK293 cells
Affiliations: Norwich Medical School, University of East Anglia, Norwich, Norfolk, United Kingdom., School of Biological Sciences, University of East Anglia, Norwich, Norfolk, United Kingdom.

Abstract:  Introduction: In contrast to the defence mechanism of RNA interference (RNAi) in plants and invertebrates, its role in the innate response to virus infection of mammals is a matter of debate. Since RNAi has a well-established role in controlling infection of the alphavirus Sindbis virus (SINV) in insects, we have used this virus to investigate the role of RNAi in SINV infection of human cells. Results: SINV AR339 and TR339-GFP were adapted to grow in HEK293 cells. Deep sequencing of small RNAs (sRNAs) early in SINV infection (4 and 6 hpi) showed low abundance (0.8%) of viral sRNAs (vsRNAs), with no size, sequence or location specific patterns characteristic of Dicer products nor did they possess any discernible pattern to ascribe to a specific RNAi biogenesis pathway. This was supported by multiple variants for each sequence, and lack of hot spots along the viral genome sequence. The abundance of the best defined vsRNAs was below the limit of Northern blot detection. The adaptation of the virus to HEK293 cells showed little sequence changes compared to the reference; however, a SNP in E1 gene with a preference from G to C was found. Deep sequencing results showed little variation of expression of cellular microRNAs (miRNAs) at 4 and 6 hpi compared to uninfected cells. Twelve miRNAs exhibiting some minor differential expression by sequencing, showed no difference in expression by Northern blot analysis. Conclusions: We show that, unlike SINV infection of invertebrates, generation of Dicer-dependent svRNAs and change in expression of cellular miRNAs were not detected as part of the Human response to SINV. 

Retracted: No

PubPeer comments:
 Figure 4B. * Blue boxes: A possible overlap in the miR196 row between the AR229 4 hpi and 6 hpi panels * Red boxes: A possible overlap in the miR197 row between the AR229 4 hpi and 6 hpi panels * There is also a thin overlap in the miR197 row between the TR339 4 hpi and 6 hpi panels, but that is not of concern.  ,
Graphene wrapped ordered LiNi0.5Mn1.5O4 nanorods as promising cathode material for lithium-ion batteries
Authors: Serguei M Aldoshin
Yanyan Qian
Jiangfeng Ni
Serguei V Savilov
Hui Xia
S Savut Jan
Xiao Tang
Journal: Scientific Reports (2015)
Discipline: Multidisciplinary
Keywords: LiNi0.5Mn1.5O4; nanorods; graphene nanosheets; cathode material; lithium-ion batteries
Affiliations: 1] School of Materials Science and Engineering, Nanjing University of Science and Technology, Nanjing 210094, China [2] Herbert Gleiter Institute of Nanoscience, Nanjing University of Science and Technology, Nanjing 210094, China., College of Physics, Optoelectronics and Energy, Soochow University, Suzhou 215006, China., Department of Chemistry, M. V. Lomonosov Moscow State University, Moscow 119991, Russia., Department of Physical Chemistry Engineering, M. V. Lomonosov Moscow State University, Moscow 119991, Russia.

Abstract:  LiNi0.5Mn1.5O4 nanorods wrapped with graphene nanosheets have been prepared and investigated as high energy and high power cathode material for lithium-ion batteries. The structural characterization by X-ray diffraction, Raman spectroscopy, and Fourier transform infrared spectroscopy indicates the LiNi0.5Mn1.5O4 nanorods prepared from Œ≤-MnO2 nanowires have ordered spinel structure with P4332 space group. The morphological characterization by scanning electron microscopy and transmission electron microscopy reveals that the LiNi0.5Mn1.5O4 nanorods of 100-200 nm in diameter are well dispersed and wrapped in the graphene nanosheets for the composite. Benefiting from the highly conductive matrix provided by graphene nanosheets and one-dimensional nanostructure of the ordered spinel, the composite electrode exhibits superior rate capability and cycling stability. As a result, the LiNi0.5Mn1.5O4-graphene composite electrode delivers reversible capacities of 127.6 and 80.8 mAh g(-1) at 0.1 and 10 C, respectively, and shows 94% capacity retention after 200 cycles at 1 C, greatly outperforming the bare LiNi0.5Mn1.5O4 nanorod cathode. The outstanding performance of the LiNi0.5Mn1.5O4-graphene composite makes it promising as cathode material for developing high energy and high power lithium-ion batteries. 

Retracted: No

PubPeer comments:
 Figure 2 shows two identical XRD patterns for difefrent samples.  , 
 #1 Fig 3.  (a) Raman spectra of the pristine graphene nanosheets, the bare LiNi0.5Mn1.5O4 nanorods and the LiNi0.5Mn1.5O4-graphene composite. (b) Enlargement of the Raman spectrum of the LiNi0.5Mn1.5O4 nanorods in the frequency range between 300 and 700u2009cmu22121. Is there a problem with the axes here? The relevant spikes are at 498 and 637 cm-1 according to 3(b), whereas in 3(a) they are located more like 600 and 750 cm-1. I have reduced (b) to the same scale as (a) and added it as an insert, to dramatise the mismatch.  ,
MiR-92b inhibited cells EMT by targeting Gabra3 and predicted prognosis of triple negative breast cancer patients
Authors: Q Jiang
Y Wang
A-P Deng
X-H Zheng
Y-Y Li
J Liu
G-Y Cheng
Q Zhou
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Triple negative breast cancer; miR-92b; Gabra3; oncogene; tumor progression
Affiliations: Department of Pharmacy, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. .

Abstract:  Objective: Triple negative breast cancer (TNBC) is a subtype of breast cancer without the three markers, which has a poor prognosis than other types. Recently, studies have identified that microRNA-92b (miR-92b) acted as potential oncogene in tumor progression, however, the biological roles of miR-92b in TNBC remain unknown. The purpose of this study was to investigate the functions of miR-92b and verify its effect on the regulation of Gabra3 in TNBC. Materials and methods: Dual-Luciferase reporter assay was recruited to confirm whether miR-92b directly binds to the 3'-untranslated region (3'-UTR) of Gabra3 mRNA in TNBC. Transwell assay was employed to analyze the capacities of migration and invasion. Western blot was applied to evaluate the expression of the special proteins that including Gabra3, epithelial-mesenchymal transition (EMT) markers and GAPDH. Results: We demonstrated that miR-92b was remarkably low expressed in TNBC tissues and cell lines, and particularly in inhibiting the migration, invasion and EMT of TNBC cells. On the contrary, Gabra3 was significantly overexpressed in TNBC tissues and cell lines in comparison with the corresponding paracancerous tissues and the normal breast epithelial cell line. The expression of miR-92b had a negative correlation with the expression of Gabra3 in TNBC tissues. Downregulation of Gabra3 could inhibit the migration, invasion and EMT of TNBC cells. MiR-92b mediated the expression of Gabra3 through directly binding to the 3'-UTR of Gabra3 mRNA. In addition, low expression of miR-92b or overexpression of Gabra3 predicted poor prognosis of TNBC patients. Conclusions: MiR-92b inhibited the migration and invasion-mediated EMT through directly targeting the 3'-UTR of Gabra3 mRNA in triple negative breast cancer. The newly identified miR-92b/Gabra3 axis may make it to be a new target for clinical diagnosis and treatment of TNBC. 

Retracted: No

PubPeer comments:
  A collection of 51 TNBC patients were included in this study from the Central Hospital of Wuhan during **2014 to 2016**, and obtained 51 pairs of cancer tissues and corresponding paracancerous tissues .  Figure 6. Identification of miR-92b and Gabra3 associated with poor survival in TNBC. A, miR-92b(-) was associated with worse outcome of TNBC patients. B, Gabra3(+) predicted poor prognosis in TNBC patients.  When this paper was published in 2019, the authors had followed patients survival for five years, i.e. through to the date range **2019-2021**. ,
The CD24 cell subset promotes invasion and metastasis in human osteosarcoma
Authors: Yan Li
Sujia Wu
Jiashi Cao
Muyu Kuang
Zhiwei Wang
Jianru Xiao
Xudong Wang
Jingjing Hu
Zhenhua Zhou
Qi Jia
Journal: EBioMedicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: Osteosarcoma; stem cell markers; CD24; tumor initiation cells; chemotherapy
Affiliations: Department of Orthopaedic Oncology, Changzheng Hospital, Naval Medical University (The Second Military Medical University), Shanghai, 200003,China., Cancer Institute, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032,China., Huadong Hospital, Fudan University, Shanghai,200040, China., Clinical Research Center, Changhai Hospital, Naval Medical University (The Second Military Medical University), Shanghai 200433, China., Department of Orthopedics, Nanjing General Hospital of Nanjing Military Region, Nanjing, Jiangsu, 210002, China., Department of Orthopedics, Changhai Hospital, Naval Medical University (The Second Military Medical University), Shanghai, 200433, China. Electronic address: ., Department of Orthopaedic Oncology, Changzheng Hospital, Naval Medical University (The Second Military Medical University), Shanghai, 200003,China. Electronic address: .

Abstract:  Background: Osteosarcoma is the most common primary aggressive bone tumor affecting children and young adolescents. Metastases are often resistant to conventional chemotherapy and mean short-term survival. Development of valuable diagnostic indicators and targeting agents will have important implications for clinical diagnosis by the identification and characterization of molecules that contribute to its aggressive behavior. Methods: We examined differential expression levels of common stem cell markers in osteosarcoma parental and sphere cells. In addition, we further analyzed the changes of candidate common stem cell markers before and after in vitro chemotherapy of osteosarcoma cells. The biological functions of CD24+ subpopulation in osteosarcoma such as proliferation, migration, invasion, tumorigenesis and metastasis were systematically investigated, and the correlations of CD24 levels with prognosis in patients with osteosarcoma were analyzed. Findings: CD24+ Cells presented characteristics of TICs and resist drug-induced apoptosis. The prevention of tumor formation and metastasis by CD24 knockdown highlights the potential of CD24 as a therapeutic target for osteosarcoma. Moreover, the levels of CD24 in osteosarcoma samples were significantly correlated with the prognosis of patients. Interpretation: CD24+ cell subset played an important role in osteosarcoma invasion and metastasis. Funding: National Natural Science Foundation of China (No.81772857); Shanghai Science and Technology Commission (18140902000); Shanghai Municipal Health Commission (2017ZZ01017; 17411950301). 

Retracted: No

PubPeer comments:
 Appears to be some image overlap within Figure 6g and 6h. See blue and red boxes respectively. Apologies if I am misunderstanding something. ***  *** Full figure, indicating location  ,
Larger-scale ocean-atmospheric patterns drive synergistic variability and world-wide volatility of wheat yields
Authors: Reza Khanbilvardi
Indrani Pal
Ehsan Najafi
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: global crop yields; predictability; climate variability; wheat yields; larger-scale climate drivers
Affiliations: Civil Engineering Department, The City College of New York, The City University of New York, New York City, 10031, USA., Advanced Science Research Center, The Graduate Center, The City University of New York, New York City, 10031, USA., NOAA Center for Earth System Sciences and Remote Sensing Technologies, The City University of New York, New York City, 10031, USA. ., The Earth Institute, Columbia University, New York City, 10025, USA. ., NOAA Center for Earth System Sciences and Remote Sensing Technologies, The City University of New York, New York City, 10031, USA.

Abstract:  Diagnosing potential predictability of global crop yields in the near term is of utmost importance for ensuring food supply and preventing socio-economic consequences. Previous studies suggest that a substantial proportion of global wheat yield variability depends on local climate and larger-scale ocean-atmospheric patterns. The science is however at its infancy to address whether synergistic variability and volatility (major departure from the normal) of multi-national crop yields can be potentially predicted by larger-scale climate drivers. Here, using observed data on wheat yields for 85 producing countries and climate variability from 1961-2013, we diagnose that wheat yields vary synergistically across key producing nations and can also be concurrently volatile, as a function of shared larger-scale climate drivers. We use a statistical approach called robust Principal Component Analysis (rPCA), to decouple and quantify the leading modes (PC) of global wheat yield variability where the top four PCs explain nearly 33% of the total variance. Diagnostics of PC1 indicate previous year's local Air Temperature variability being the primary influence and the tropical Pacific Ocean being the most dominating larger-scale climate stimulus. Results also demonstrate that world-wide yield volatility has become more common in the current most decades, associating with warmer northern Pacific and Atlantic oceans, leading mostly to global supply shortages. As the world warms and extreme weather events become more common, this diagnostic analysis provides convincing evidence that concurrent variability and world-wide volatility of wheat yields can potentially be predicted, which has major socio-economic and commercial importance at the global scale, underscoring the urgency of common options in managing climate risk. 

Retracted: No

PubPeer comments:
  I ve noticed some unusual similarities within this figure from the paper. ,
The anthelmintic flubendazole blocks human melanoma growth and metastasis and suppresses programmed cell death protein-1 and myeloid-derived suppressor cell accumulation
Authors: Mina Elahy
Hong Xin
Grishma Acharya
Levon M Khachigian
Yue Li
Journal: Cancer Letters (2019)
Discipline: CLINICAL MEDICINE
Keywords: Flubendazole; Melanoma; Myeloid-derived suppressor cells; Programmed cell death protein-1.
Affiliations: Vascular Biology and Translational Research, School of Medical Sciences, UNSW Medicine, University of New South Wales, Sydney, NSW, 2052, Australia., Explora BioLabs, Flintkote Avenue, San Diego, CA, 92121, USA., Vascular Biology and Translational Research, School of Medical Sciences, UNSW Medicine, University of New South Wales, Sydney, NSW, 2052, Australia. Electronic address: .

Abstract:  The incidence of melanoma is increasing faster than any other cancer. In recent years, treatment of melanoma and a range of other deadly cancers has involved immunotherapy with programmed cell death protein-1 (PD-1)/PD-1 ligand (PD-L1) checkpoint blockade which has improved survival. However, many patients do not respond or have partial response, survival benefit is in the order of months and all available PD-1/PD-L1 strategies are antibodies requiring intravenous infusion. There are no clinically approved small molecule pharmacologic inhibitors of the PD-1/PD-L1 system. The benzimidazole derivative flubendazole is a widely used anthelmintic available over the counter in Europe. Here we demonstrate the ability of flubendazole to inhibit human melanoma growth and spread in mice. Flubendazole's ability to block tumor growth and spread was comparable to paclitaxel. Anti-tumor effects were observed when flubendazole was delivered systemically not locally. Flubendazole inhibited CD31/PECAM-1 staining indicating suppression of tumor angiogenesis. Most surprisingly, flubendazole inhibited PD-1 levels within the tumors, but not PD-L1. Western blotting and flow cytometry revealed that flubendazole inhibits PD-1 expression in cultured melanoma cells. Flubendazole also reduced myeloid-derived suppressor cell (MDSC) levels in tumor tissue. Further we found that flubendazole inhibited active (phospho-Tyr705) signal transducer and activator of transcription (STAT3), an upstream regulator of PD-1 expression. These findings uncover that flubendazole is a novel small molecule inhibitor of not only melanoma growth and spread but also of PD-1 and MDSC. 

Retracted: No

PubPeer comments:
 What are the error bars in Fig. 1A,B Fig. 2B,C Fig.3 A,B Fig. 4 A,B,C,D,E ? It is not stated in the legends or in the Materials and methods. This makes it difficult to interpret the data, and if you look for the underlying data so you can do the statistics yourself, in Appendix A. Supplementary data it says  Data not available The data that has been used is confidential . ,
Metabolic Reprogramming of Pancreatic Cancer Mediated by CDK4/6 Inhibition Elicits Unique Vulnerabilities
Authors: Elizaveta Freinkman
Uthra Balaji
Jorge Franco
Agnieszka K Witkiewicz
Erik S Knudsen
Journal: Cell Reports (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p16ink4a; pancreatic ductal adenocarcinoma; CDK4/6; cell cycle; ATP
Affiliations: McDermott Center University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA., Whitehead Institute, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA., McDermott Center University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA; Simmons Cancer Center, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA. Electronic address: .

Abstract:  Due to loss of p16ink4a in pancreatic ductal adenocarcinoma (PDA), pharmacological suppression of CDK4/6 could represent a potent target for treatment. In PDA models, CDK4/6 inhibition had a variable effect on cell cycle but yielded accumulation of ATP and mitochondria. Pharmacological CDK4/6 inhibitors induce cyclin D1 protein levels; however, RB activation was required and sufficient for mitochondrial accumulation. CDK4/6 inhibition stimulated glycolytic and oxidative metabolism and was associated with an increase in mTORC1 activity. MTOR and MEK inhibitors potently cooperate with CDK4/6 inhibition in eliciting cell-cycle exit. However, MTOR inhibition fully suppressed metabolism and yielded apoptosis and suppression of tumor growth in xenograft models. The metabolic state mediated by CDK4/6 inhibition increases mitochondrial number and reactive oxygen species (ROS). Concordantly, the suppression of ROS scavenging or BCL2 antagonists cooperated with CDK4/6 inhibition. Together, these data define the impact of therapeutics on PDA metabolism and provide strategies for converting cytostatic response to tumor cell killing. 

Retracted: No

PubPeer comments:
 Figure 4E appears to include a repeated image. ***  , 
 Thank you for pointing this out!!! I have contacted the journal for correction. , 
 #2 Thank you for responding and addressing this concern. , 
 Erratum dated 2020-07-07 (Cell Reports 14, 979u2013990; February 9, 2016) In the originally published version of this article, there was an inadvertent duplication of the single agent controls in Figure 1E. A corrected version of the figure panel is provided here. The authors regret this error. ***  ,