PReD-Bench/PRed-Bench huggingface dataset:
The transcriptional regulator BBX24 impairs DELLA activity to promote shade avoidance in Arabidopsis thaliana
Authors: Cristian M Escudero
Carlos D Crocco
David Alabad√≠
Miguel A Bl√°zquez
Antonella Locascio
Javier F Botto
Journal: Nature Communications (2015)
Discipline: Multidisciplinary
Keywords: Canopy shade; Plant response; PIF4; BBX24; DELLA proteins
Affiliations: IFEVA, Facultad de Agronom√≠a, Universidad de Buenos Aires y Consejo Nacional de Investigaciones Cient√≠ficas y T√©cnicas, Avenue San Mart√≠n 4453, Buenos Aires C1417DSE, Argentina., 1] Instituto de Biolog√≠a Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cient√≠ficas-Universidad Polit√©cnica de Valencia, Valencia 46022, Spain [2] Department of Agronomy, Food, Natural Resources, Animals and the Environment (DAFNAE), Padova University, Viale dell'Universit√° 16, Legnaro 35020, Italy., Instituto de Biolog√≠a Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cient√≠ficas-Universidad Polit√©cnica de Valencia, Valencia 46022, Spain.

Abstract:  In response to canopy shade, plant vegetative structures elongate to gain access to light. However, the mechanism that allows a plastic transcriptional response to canopy shade light is not fully elucidated. Here we propose that the activity of PIF4, a key transcription factor in the shade signalling network, is modulated by the interplay between the BBX24 transcriptional regulator and DELLA proteins, which are negative regulators of the gibberellin (GA) signalling pathway. We show that GA-related targets are enriched among genes responsive to BBX24 under shade and that the shade-response defect in bbx24 mutants is rescued by a GA treatment that promotes DELLA degradation. BBX24 physically interacts with DELLA proteins and alleviates DELLA-mediated repression of PIF4 activity. The proposed molecular mechanism provides reversible regulation of the activity of a key transcription factor that may prove especially relevant under fluctuating light conditions. 

Retracted: No

PubPeer comments:
 Figure 4A and 4B, much more similar than expected (boxes of same color). Resolution of yeast strips in Fig. 4A is suboptimal, but they seem to be the same strips. Could the authors please check and post the images at higher resolution in order to take away any concern?  ,
LncRNA AB073614 induces epithelial- mesenchymal transition of colorectal cancer cells via regulating the JAK/STAT3 pathway
Authors: Jinfang Xue
Fang Yin
Haoyu Kuang
Yanan Wang
Liya Liao
Xiaojun Zhou
Journal: Cancer Biomarkers (2018)
Discipline: CLINICAL MEDICINE
Keywords: Colorectal cancer; JAK/STAT3; LncRNA AB073614; epithelial-mesenchymal transition.
Affiliations: Department of Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai 519000, Guangdong, China., Department of General Surgery, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai 519000, Guangdong, China., Department of Gastroenterology, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai 519000, Guangdong, China.

Abstract:  Background: LncRNAs are involved in the metastasis and recurrence of human tumors, including colorectal cancer (CRC). We previously reported that lncRNA AB073614 promotes tumor proliferation and metastasis and predicted a poor clinical outcome of CRC patients. Herein, we investigated the underlying mechanism of lncRNA AB073614-related metastasis in CRC. Material and methods: The expression of lncRNA AB073614 in CRC tissues were evaluated by quantitative real-time PCR (qRT-PCR). Transwell assay was performed to detect the effects of lncRNA AB073614 on cell migration and invasion. Epithelial-mesenchymal transition (EMT) molecular markers and Janus kinase/signal transducer and activator of transcription (JAK/STAT3) pathway proteins expression levels were detected by Western blot and Immunofluorescence. Results: We confirmed that lncRNA AB073614 was highly expressed in the colorectal cancer tissues. LncRNA AB073614 knockdown in SW480 and HCT116 cells significantly promoted the protein expression levels of E-cadherin and Occludin, and decreased the expressions of N-cadherin and Vimentin, then further decreased the cell migration and invasion ability. Interestingly, the expression of phosphorylated STAT3 was also down-regulated. Furthermore, SW480 and HCT116 cells were transfected with lncRNA AB073614 vector and treated with a JAK inhibitor, AT9283. The results showed that lncRNA AB073614 regulated EMT through JAK-STAT3 signaling pathway. Conclusion: All these results indicate that lncRNA AB073614 can induce the expression of EMT cell markers and regulate the process of EMT of CRC cells through regulating the JAK/STAT3 pathway activation. 

Retracted: No

PubPeer comments:
 Could the authors please review Figure 2 in the published version of this paper? The copy I have is a  proof and in that version there appears to be a repeated image. Thank you. TAM ***  ,
Role of DNA methylation in cell cycle arrest induced by Cr (VI) in two cell lines
Authors: Kecheng Liu
Jianlin Lou
Xiuzhi Wang
Yufeng Tan
Peng Song
Xing Zhang
Yu Wang
Lingzhi Jin
Chunji Yao
Nanxiang Wu
Ming Gao
Yun Xiao
Yang Song
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Hexavalent chromium; carcinogenicity; DNA methylation; cell cycle; global hypomethylation
Affiliations: Institute of Hygiene, Zhejiang Academy of Medical Sciences, Hangzhou, Zhejiang, People's Republic of China. 

Abstract:  Hexavalent chromium [Cr(IV)], a well-known industrial waste product and an environmental pollutant, is recognized as a human carcinogen. But its mechanisms of carcinogenicity remain unclear, and recent studies suggest that DNA methylation may play an important role in the carcinogenesis of Cr(IV). The aim of our study was to investigate the effects of Cr(IV) on cell cycle progress, global DNA methylation, and DNA methylation of p16 gene. A human B lymphoblastoid cell line and a human lung cell line A549 were exposed to 5-15 ¬µM potassium dichromate or 1.25-5 ¬µg/cm¬≤ lead chromate for 2-24 hours. Cell cycle was arrested at G‚Ç?phase by both compounds in 24 hours exposure group, but global hypomethylation occurred earlier than cell cycle arrest, and the hypomethylation status maintained for more than 20 hours. The mRNA expression of p16 was significantly up-regulated by Cr(IV), especially by potassium dichromate, and the mRNA expression of cyclin-dependent kinases (CDK4 and CDK6) was significantly down-regulated. But protein expression analysis showed very little change of p16 gene. Both qualitative and quantitative results showed that DNA methylation status of p16 remained unchanged. Collectively, our data suggested that global hypomethylation was possibly responsible for Cr(IV)-induced G‚Ç?phase arrest, but DNA methylation might not be related to up-regulation of p16 gene by Cr(IV). 

Retracted: No

PubPeer comments:
 Figure 3. Reported to the journal in October 2015. Several lanes in all four panels show unexpected uniform grey backgrounds or patches. Indicated with green arrows.  ,
Somatostatin derivative (smsDX) targets cellular metabolism in prostate cancer cells after androgen deprivation therapy
Authors: Zhaoquan Xing
Wei Jiao
Zhaoxu Liu
Zhonghua Xu
Zhenghui Fang
Zhiqing Fang
Lei Yan
Zhaoxin Guo
Xiaoyu Guo
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Cancer cell metabolism; Androgen deprivation therapy; Prostate cancer; LNCaP-s cells; Castration-resistant prostate cancer
Affiliations: Department of Urology, Qilu Hospital, Shandong University, Jinan, China.

Abstract:  Cancer cell metabolism responsive to androgen deprivation therapy (ADT) may be involved in the development and progression of prostate cancer and the ultimate failure of androgen-deprivation therapy. To investigate the metabolism regulation effects on androgen-independent growth of prostate cancer, an established LNCaP-s cell model that resembles the clinical scenario of castration-resistant prostate cancer (CRPC), was used in this current study. This cell line was cultured from androgen-sensitive LNCaP parental cells, in an androgen-reduced condition, resembling clinical androgen deprivation therapy. To assess the effects of smsDX on the invasiveness of prostate cancer cells we used wound healing assay and Matrigel‚Ñ?invasion assay. We evaluated differentially expressed proteins of the parental LNCaP cells and LNCaP-s cells after ADT by means of two-dimensional gel electrophoresis (2-DE) followed by MALDI-TOF mass spectrometric analysis. The covered area in the wound and the number of cells invading through a Matrigel chamber were significantly smaller for cells treated with smsDX than they were for control cells treated with vehicle. 56 proteins were found differentially expressed in LNCaP-s cells compared to LNCaP cells, majority of them were down-regulated after ADT treatment. 104 proteins of LNCaP cells and 86 in LNCaP-s cells, separately, were found differentially expressed after treatment with smsDX, When we explored these protein functions within the website UniProtKB/Swiss-Prot, surprisingly, most of the proteins were found to be involved in the cellular metabolism and mitochondrial function regulation. LNCaP-s as potential metastatic androgen-independent cancer cells, its metabolism and mitochondrial functions could be altered by a new somatostatin derivative smsDX, the smsDX regulatory effects on metabolism in LNCaP-s deliver more therapeutic information with the treatment of CRPC. 

Retracted: No

PubPeer comments:
 Figure 2B. * Red boxes: two panels appear to share an overlap.  ,
Intravenous injection of neural progenitor cells facilitates angiogenesis after cerebral ischemia
Authors: Kouichi Tanonaka
Norio Takagi
Yoshiyuki Moriyama
Kanae Hashimura
Chisa Itokawa
Journal: Brain and Behavior (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Angiopoietin; VEGF; cerebral ischemia; neural progenitor cells; tight junctional protein.
Affiliations: Department of Molecular and Cellular Pharmacology; Tokyo University of Pharmacy and Life Sciences; 1432-1 Horinouchi Hachioji Tokyo 192-0392 Japan

Abstract:  Earlier we demonstrated that the injection of neural progenitor cells (NPCs) has therapeutic potential for the improvement of learning dysfunction after cerebral ischemia. However, it remained to be clarified how transplantation of NPCs can improve ischemia-induced dysfunction. In this study, we examined whether intravenous injection of NPCs after cerebral ischemia could enhance angiogenesis by affecting the expression of angiogenic factors. The injection of NPCs on day 7 after cerebral ischemia enhanced angiogenesis on day 28. Vascular endothelial growth factor (VEGF) and its receptor VEGFR2 were increased in expression by the NPC injection. The level of angiopoietin-1 (Ang-1), an angiogenic factor, but not that of Ang-2, which acts as an antagonist for the Ang-1 receptor, was also increased on day 28. In addition, the expression of Ang-1 receptor Tie2 was enhanced in brain capillaries. Furthermore, the amounts of tight junctional proteins, which are in the blood-brain barrier and whose expression occurs downstream of Ang-1/Tie2 signaling, were increased by the NPC injection. These results suggest that the NPC injection promoted angiogenesis through Ang-1/Tie2 and/or VEGF/VEGFR2 signaling in brain capillaries after cerebral ischemia. Such signaling might have the potential for causing vascular stabilization and maturation for a long period after cerebral ischemia. 

Retracted: No

PubPeer comments:
 The same beta-actin bands were used in Figure 5A and B:  The same beta-actin bands in Figures 6, 7A, and 7B (all Day 28, Day 7 only for Figure 6 and 7A):  ,
MiR-103 alleviates autophagy and apoptosis by regulating SOX2 in LPS-injured PC12 cells and SCI rats
Authors: Guowei Li
Tao Chen
Xiaoyu Xiao
Yingxian Zhu
Zongwen Huang
Juyuan Bu
Journal: Iranian journal of basic medical sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Apoptosis; Autophagy; MAPK/ERK and JAK/STAT -pathway; MiR-103; SOX2
Affiliations: Department of Spine Surgery, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong 519000, China., Department of Anaesthesiology, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong 519000, China., Department of Gastroenterological Surgery, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong 519000, China.

Abstract:  Objectives: Recent studies revealed that microRNAs (miRNAs) may play crucial roles in the responses and pathologic processes of spinal cord injury (SCI). This study aimed to investigate the effect and the molecular basis of miR-103 on LPS-induced injuries in PC12 cells in vitro and SCI rats in vivo. Materials and methods: PC12 cells were exposed to LPS to induce cell injuries to mimic the in vitro model of SCI. The expression of miR-103 and SOX2 in PC12 cells were altered by transient transfections. Cell viability and apoptotic cell rate were measured by CCK-8 assay and flow cytometry assay. Furthermore, Western blot analysis was performed to detect the expression levels of apoptosis- and autophagy- related proteins, MAPK/ERK pathway- and JAK/STAT pathway-related proteins. In addition, we also assessed the effect of miR-103 agomir on SCI rats. Results: LPS exposure induced cell injuries in PC12 cells. miR-103 overexpression significantly increased cell viability, reduced cell apoptosis and autophagy, and opposite results were observed in miR-103 inhibition. miR-103 attenuated LPS-induced injuries by indirect upregulation of SOX2. SOX2 overexpression protected PC12 cells against LPS-induced injuries, while SOX2 inhibition expedited LPS-induced cell injuries. Furthermore, miR-103 overexpression inhibited MAPK/ERK pathway and JAK/STAT pathway through upregulation of SOX2. We also found that miR-103 agomir inhibited cell apoptosis and autophagy in SCI rats. Conclusion: This study demonstrates that miR-103 may represent a protective effect against cell apoptosis and autophagy in LPS-injured PC12 cells and SCI rats by upregulation of SOX2 expression. 

Retracted: No

PubPeer comments:
 This paper conforms to a style identified by [Dr Elisabeth Bik] and [Dr Jana Christopher] , among others. Shown here are Figs 6A B.  ,
Chinese herbal medicine suppresses invasion-promoting capacity of cancer-associated fibroblasts in pancreatic cancer
Authors: Litao Xu
Chao Qu
Kun Wang
Zhen Chen
Luming Liu
Peng Wang
Zhiqiang Meng
Hao Chen
Jianmin Luo
Lianyu Chen
Qi Qi
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Pancreatic cancer; Qingyihuaji; Chinese medicine; cancer-associated fibroblast; CAF
Affiliations: Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China; Department of Oncology, Shanghai medical college, Fudan University, Shanghai, China., Department of Oncology, Shanghai medical college, Fudan University, Shanghai, China.

Abstract:  Pancreatic cancer remains one of the leading causes of cancer-related deaths, due to aggressive growth, high metastatic rates during the early stage and the lack of an effective therapeutic approach. We previously showed that Qingyihuaji (QYHJ), a seven-herb Chinese medicine formula, exhibited significant anti-cancer effects in pancreatic cancer, associated with modifications in the tumor microenvironment, particularly the inhibition of cancer-associated fibroblast (CAF) activation. In the present study, we generated CAF and paired normal fibroblast (NF) cultures from resected human pancreatic cancer tissues. We observed that CAFs exhibited an enhanced capacity for inducing pancreatic cancer cell migration and invasion compared with NFs, while QYHJ-treated CAFs exhibited decreased migration and invasion-promoting capacities in vitro. The results of further analyses indicated that compared with NFs, CAFs exhibit increased CXCL1, 2 and 8 expression, contributing to the enhanced invasion-promoting capacities of these cells, while QYHJ treatment significantly suppressed CAF proliferation activities and the production of CAF-derived CXCL1, 2 and 8. These in vitro observations were confirmed in mice models of human pancreatic cancer. Taken together, these results suggested that suppressing the tumor-promoting capacity of CAFs through Chinese herbal medicine attenuates pancreatic cancer cell invasion. 

Retracted: No

PubPeer comments:
 Figure 5, bottom left panels. * Red boxes: In the Invasion row, the Vehicle and XCCL8.anti CXCR1 Ab panels appear to show an overlap.  , 
 Figure S2, left panels. * Orange boxes: The #1 and #2 CAF (Ctrl-treated) invasion panels appear to show an overlap. It is not clear how these two differ, but I will assume for now these are different cell lines cell types experiments. Maybe the authors can clarify, please?  ,
Acrolein induces apoptosis through the death receptor pathway in A549 lung cells: role of p53This review is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease
Authors: Pragathi Pallepati
Ahmed Bettaieb
Diana A Averill-Bates
Julie Roy
Journal: Canadian Journal of Physiology and Pharmacology (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Acrolein; Apoptosis; p53; Death receptor pathway; Fas ligand
Affiliations: D√©partement des sciences biologiques, TOXEN, Universit√© du Qu√©bec √† Montr√©al, CP 8888, Succursale Centre Ville, Montr√©al, QC H3C¬†3P8, Canada.

Abstract:  Acrolein, a highly reactive alpha,beta-unsaturated aldehyde, is an omnipresent environmental pollutant. Chronic and acute human exposures occur through exogenous and endogenous sources, including food, vapors of overheated cooking oil, house and forest fires, cigarette smoke, and automobile exhaust. Acrolein is a toxic byproduct of lipid peroxidation, which has been implicated in pulmonary, cardiac, and neurodegenerative diseases. This study shows that p53 is an initiating factor in acrolein-induced death receptor activation during apoptosis in A549 human lung cells. Exposure of cells to acrolein (0-50 micromol/L) mainly caused apoptosis, which was manifested by execution phase events such as condensation of nuclear chromatin, phosphatidylserine externalization, and poly(ADP-ribose) polymerase (PARP) cleavage. Levels of necrosis (approximately 5%) were low. Acrolein triggered the death receptor pathway of apoptosis, causing elevation of Fas ligand (FasL) and translocation of adaptor protein Fas-associated death domain to the plasma membrane. Acrolein caused activation of caspase-8, caspase-2, caspase-7, and the cross-talk pathway mediated by Bid cleavage. Activation of p53 and increased expression of p53-upregulated modulator of apoptosis (PUMA) occurred in response to acrolein. FasL upregulation and caspase-8 activation were decreased by p53 inhibitor pifithrin-alpha and antioxidant polyethylene glycol catalase. These findings increase our knowledge about the induction of cell death pathways by acrolein, which has important implications for human health. 

Retracted: No

PubPeer comments:
 Concern about Figure 8C. * Pink arrows: splice lines appear to be visible between the first and second, and between the fourth and the fifth lane * Green arrows: a horizontal splice line might be visible in the second, third, and fifth lanes. * Yellow boxes: The 85 kDa band in the first lane looks like that in the fifth lane. As noted above, some straight background transition lines appear be visible around the latter. * Blue boxes: The top bands in the second and fifth lane look very similar. Could the authors take away any concerns by showing the original blot, please?  ,
Effects of THAP11 on erythroid differentiation and megakaryocytic differentiation of K562 cells
Authors: Jian-Jie Li
Chang-Hui Ge
Hui Chen
Xiao-Ming Yang
Fei-Fei Xu
Yang Yang
Hong-Mei Ning
Xiang-Zhen Kong
Miao Yu
Chang-Yan Li
Xiao-Ming Dong
Wei-Wei Zheng
Jian-Hong Zhang
Rong-Hua Yin
Yi-Qun Zhan
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Hematopoiesis; THAP11; differentiation; transcription factors; erythroid
Affiliations: Department of Pharmaceutical Engineering, Tianjin University, Tianjin, China; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China., Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China; State Key Laboratory of Proteomics, Beijing, China., Department of Hematopoietic Stem Cell Transplantation, Affiliated Hospital to Academy of Military Medical Sciences, Beijing, China., Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China., Department of Pharmaceutical Engineering, Tianjin University, Tianjin, China., Department of Chemistry, Purdue University, West Lafayette, Indiana, United States of America., Department of Pulmonary Neoplasms Internal Medicine, Affiliated Hospital to Academy of Military Medicine Sciences, Beijing, China., Department of Pharmaceutical Engineering, Tianjin University, Tianjin, China; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China; State Key Laboratory of Proteomics, Beijing, China.

Abstract:  Hematopoiesis is a complex process regulated by sets of transcription factors in a stage-specific and context-dependent manner. THAP11 is a transcription factor involved in cell growth, ES cell pluripotency, and embryogenesis. Here we showed that THAP11 was down-regulated during erythroid differentiation but up-regulated during megakaryocytic differentiation of cord blood CD34+ cells. Overexpression of THAP11 in K562 cells inhibited the erythroid differentiation induced by hemin with decreased numbers of benzidine-positive cells and decreased mRNA levels of Œ±-globin (HBA) and glycophorin A (GPA), and knockdown of THAP11 enhanced the erythroid differentiation. Conversely, THAP11 overexpression accelerated the megakaryocytic differentiation induced by phorbol myristate acetate (PMA) with increased percentage of CD41+ cells, increased numbers of 4N cells, and elevated CD61 mRNA levels, and THAP11 knockdown attenuated the megakaryocytic differentiation. The expression levels of transcription factors such as c-Myc, c-Myb, GATA-2, and Fli1 were changed by THAP11 overexpression. In this way, our results suggested that THAP11 reversibly regulated erythroid and megakaryocytic differentiation. 

Retracted: No

PubPeer comments:
 Great to see that circadian variation in the breathalome is getting more attention. A relevant reference from 2014: https: doi.org 10.1371 journal.pone.0114422 ,
CD137-CD137L interaction modulates neointima formation and the phenotype transformation of vascular smooth muscle cells via NFATc1 signaling
Authors: Jinchuan Yan
Zhongqun Wang
Chen Shao
Cuiping Wang
Wei Zhong
Wei Yuan
Ping Yang
Rui Chen
Bo Li
Journal: Molecular and cellular biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Atherosclerosis; CD137; NFATc1; Phenotype; VSMC.
Affiliations: Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, People's Republic of China., Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, People's Republic of China. .

Abstract:  Vascular smooth muscle cell (VSMC) phenotype transformation is an important event in the formation of vessel neointima during lesion progression. CD137 can accelerate plaque formation, but the underlying mechanisms of this process remain unknown. Thus, we investigated the effect of CD137 signaling on VSMC phenotype transformation and potential mechanism underlying this transformation. Mouse recombinant CD137L and anti-CD137 antibody were used to activate or block the CD137 signaling way, respectively. Real-time PCR, immunofluorescence, and western blot analyses were performed to detect the expression of NFATc1 and phenotype markers such as SM-MHC, Œ±-SMA, and vimentin in vivo or in vitro. Inhibition of NFATc1 expression was established by small interfering RNA (siRNA) and lentivirus in vitro and in vivo, respectively. Plenti-virus vector was constructed to overexpress NFATc1. Transwell assay was used to detect the migration ability of cells. The expression of NFATc1 was significantly upregulated by treating VSMCs with CD137L. The contractile phenotype markers decreased, while the synthesis phenotype marker and cell migration increased after CD137 stimulation. This phenomenon can be blocked by combined use of anti-CD137 antibody or siRNA of NFATc1. Overexpression of NFATc1 caused the VSMC phenotype transformation independently. In conclusion, the CD137-CD137L pathway plays an important role in regulating VSMC phenotype transformation via activation of NFATc1 signaling pathway. 

Retracted: No

PubPeer comments:
  ,
Propofol inhibits proliferation and epithelial-mesenchymal transition of MCF-7 cells by suppressing miR-21 expression
Authors: Qing Du
Hongmei Xu
Xin Zhang
Ming Wei
Xuezhi Zhang
Shilei Wang
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MCF-7; Propofol; epithelial-mesenchymal transition (EMT); miR-21.
Affiliations: a Department of Anesthesiology , The Affiliated Hospital of Qingdao University , Qingdao , China., b Emergency Department , The Affiliated Hospital of Qingdao University , Qingdao , China.

Abstract:  Breast cancer is a common malignant tumor with a high incidence of recurrence and metastasis. It has been reported that propofol has certain anti-breast cancer effects, but the intrinsic molecular mechanism remains unclear. This study investigated the effect of propofol on breast cancer MCF-7 cells and its possible regulatory mechanisms. MCF-7 cells were treated by propofol, and then the effects of propofol on cell growth and epithelial-mesenchymal transition (EMT) were studied. We subsequently testified whether miR-21 was a downstream effector of propofol. As a result, propofol repressed the proliferation and migration of MCF-7 cells, but significantly induced apoptosis. Meanwhile, miR-21 expression and EMT were inhibited by propofol stimulation. The effects of propofol on MCF-7 cells proliferation, apoptosis and EMT were all attenuated when miR-21 was overexpressed. Besides this, the activation of PI3K/AKT and Wnt3a/Œ≤-catenin pathways was reduced by propofol stimulation in a miR-21-depedent manner. In conclusion, propofol can inhibit the proliferation and EMT of MCF-7 cells by down-regulating miR-21 expression. Moreover, miR-21 can further regulate PI3K/AKT and Wnt/Œ≤-catenin pathways. 

Retracted: No

PubPeer comments:
 Figure 6. Much more similar than expected. https: imgur.com IB9hz6F ,
Long-term electromagnetic pulse exposure induces Abeta deposition and cognitive dysfunction through oxidative stress and overexpression of APP and BACE1
Authors: Hai-Yang Lang
Jin-Hui Li
Jie Zhang
Guo-Zhen Guo
Guang-Zhou An
Jing Li
Da-Peng Jiang
Sheng-Long Xu
Ya-Feng Wang
Fang Kuang
Journal: Brain Research (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer◊≥s disease; Autophagy; BACE1; Electromagnetic pulse; Oxidative stress
Affiliations: Department of Radiation medicine, Fourth Military Medical University, China., Institute of Disease Control and Prevention, Academy of Military Medical Science, China., Institute of neurosciences, Fourth Military Medical University, China., Navy Center for Disease Control and Prevention, China., Department of Radiation medicine, Fourth Military Medical University, China. Electronic address: .

Abstract:  A progressively expanded literature has been devoted in the past years to the noxious or beneficial effects of electromagnetic field (EMF) to Alzheimer◊≥s disease (AD). This study concerns the relationship between electromagnetic pulse (EMP) exposure and the occurrence of AD in rats and the underlying mechanisms, focusing on the role of oxidative stress (OS). 55 healthy male Sprague Dawley (SD) rats were used and received continuous exposure for 8 months. Morris water maze (MWM) test was conducted to test the ability of cognitive and memory. The level of OS was detected by superoxide dismutase (SOD) activity and glutathione (GSH) content. We found that long-term EMP exposure induced cognitive damage in rats. The content of Œ≤-amyloid (AŒ≤) protein in hippocampus was increased after long-term EMP exposure. OS of hippocampal neuron was detected. Western blotting and immunohistochemistry (IHC) assay showed that the content of AŒ≤ protein and its oligomers in EMP-exposed rats were higher than that of sham-exposed rats. The content of Beta Site App Cleaving Enzyme (BACE1) and microtubule-associated protein 1 light chain 3-II (LC3-II) in EMP-exposed rats hippocampus were also higher than that of sham-exposed rats. SOD activity and GSH content in EMP-exposed rats were lower than sham-exposed rats (p&lt;0.05). Several mechanisms were proposed based on EMP exposure-induced OS, including increased amyloid precursor protein (APP) aberrant cleavage. Although further study is needed, the present results suggest that long-term EMP exposure is harmful to cognitive ability in rats and could induce AD-like pathological manifestation. 

Retracted: No

PubPeer comments:
 Figure 4C is just a mirror image of figure 3D, even though they are supposedly showing staining of AB expression or AB oligomer expression, and are from two separate treatment samples (different frequency pulse exposures).  ,
TUG1/miR-133b/CXCR4 axis regulates cisplatin resistance in human tongue squamous cell carcinoma
Authors: Ke Zhang
Xuanping Cao
Bo Yan
Hong Zhou
Journal: Cancer cell international (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CXCR4; Cisplatin resistance; TSCC; TUG1; miR-133b.
Affiliations: The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450000 Henan China.

Abstract:  Background: Long noncoding RNA taurine upregulated 1 (TUG1) has been reported to play an important role in human cancers. However, little is known about the role of TUG1 in drug resistance and its mechanism in tongue squamous cell carcinoma (TSCC). Methods: Twenty-one cisplatin-sensitive or resistant TSCC patients were enrolled in this study. Cisplatin-resistant cells (SCC25/CDDP and CAL27/CDDP) were used for experiments in vitro. Transfection was performed using Lipofectamine 2000 transfection reagent. The levels of TUG1, microRNA-133b (miR-133b) and cysteine-X-cysteine chemokine receptor 4 (CXCR4) were measured by quantitative real-time polymerase chain reaction or western blot. The cisplatin resistance was investigated by cell viability, transwell invasion and apoptosis assays. The interactions among TUG1, miR-133b and CXCR4 were evaluated by luciferase reporter assay and RNA immunoprecipitation. Murine xenograft model was established using the stably transfected CAL27/CDDP cells. Results: TUG1 expression was elevated in cisplatin-resistant TSCC tissues and cells compared with that in sensitive group and its knockdown inhibited cisplatin resistance to SCC25/CDDP and CAL27/CDDP cells. miR-133b was targeted via TUG1 and its overexpression suppressed cisplatin resistance. Moreover, CXCR4 was a target of miR-133b. CXCR4 silence repressed cisplatin resistance, which was reversed by miR-133b knockdown. The level of CXCR4 protein was decreased by inhibition of TUG1 and recuperated by miR-133b knockdown. Besides, interference of TUG1 attenuated tumor growth by regulating miR-133b and CXCR4 in vivo. Conclusion: Downregulation of TUG1 impeded cisplatin resistance in TSCC-resistant cells by mediating miR-133b and CXCR4, indicating TUG1 as a promising target for TSCC chemotherapy. 

Retracted: No

PubPeer comments:
 All the western immunoblots in this article look artificial: the bands are blurry and there is lack of any background noise. If you increase the contrast, the background is completely empty:  , 
 Another paper by the same lead author was published in an e-Century journal -- without a DOI or a PubMed ID, which rules out a separate PubPeer thread for it. I will mention it here instead, as it displays similar Miro-blob-like WBs: [ miRNA-126b regulated apoptosis of the human tongue carcinoma cell line Tca8113-P60 via P38 signaling pathway ](http: www.ijcem.com files ijcem0037176.pdf) (Yingqi Zhang, Weili Liu, Hongli Wang, Bo Xu, Hua Li Xuanping Cao, 2017). Fig 4A:  That paper is also of interest for its Fig 2A:  MiRNA-126b induced cell surface expression of phosphatidylserine. A: Representative graph of flow cytometry analysis of phosphatidylserine expression in different groups.   ,
LncRNA NEAT1 reversed the hindering effects of miR-495-3p/STAT3 axis and miR-211/PI3K/AKT axis on sepsis-relevant inflammation
Authors: Panyu Zhou
Yan Xia
Chen Wang
Demeng Xia
Renqi Yao
Shuogui Xu
Journal: Molecular Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: Inflammation; LncRNA; Mice model; NEAT1; RAW264.7
Affiliations: Department of Emergency, Changhai Hospital, Naval Medical University, Shanghai, China., Department of Burn, Changhai Hospital, Naval Medical University, Shanghai, China., Department of Emergency, Changhai Hospital, Naval Medical University, Shanghai, China. Electronic address: .

Abstract:  Objective: This investigation was intended to elucidate lncRNA-miRNA networks that could explain inflammation underlying sepsis progression. Methods: In the first place, four kinds of mice models were established, namely, SHAM group (n = 30), trauma (TH) group (n = 30), lipopolysaccharide (LPS) group (n = 30) and TH + LPS group (n = 30). Their lung, spleen and liver tissues were gathered for determination of TNF-Œ±, IL-6, IL-10 and MCP-1 levels. Furthermore, mouse mononuclear macrophage leukemia cell line (RAW264.7) was stimulated by LPS to establish inflammation cell models. Then si-NEAT1s, pcDNA3.1-NEAT1, miR-495-3p mimic, miR-495-3p inhibitor, miR-NC, miR-211 mimic and miR-211 inhibitor were, respectively, transfected into the cells, so as to observe the impacts of NEAT1, miR-495-3p and miR-211 on cytokine levels released by the cells. Results: The survival condition of mice in the TH + LPS group was undesirable, in relative to mice in the LPS group and SHAM group (both P &lt; 0.05). High-level NEAT1 and low-level miR-495-3p/miR-211 were associated with poor survival of mice in the TH+LPS group (P &lt; 0.05). Additionally, the correlation between NEAT1/miR-495-3p/miR-211 level and cytokine level was the strongest among TH+LPS-treated mice, in comparison to mice treated by TH or LPS. Furthermore, up-regulation of NEAT1 level and down-regulation of miR-495-3p/miR-211 level could aggravate inflammation in LPS-treated RAW264.7 cells. The miR-495-3p and miR-211 herein, were both subjected to sponging of NEAT1, possibly affected inflammation responses in RAW264.7 cells, respectively, through modulating STAT3 and PI3K/AKT signaling. Conclusion: LncRNA NEAT1 exhibited great potential sepsis diagnosis and treatment, considering its modifying miR-495-3p/STAT3 axis and miR-211/PI3K/AKT axis in inflammation cell models. 

Retracted: No

PubPeer comments:
 The Western immunoblots in this paper look artificial. They have no background. The description in the Materials and Methods is also unusual, eg. at the end of the section  Western blotting :  Eventually, electro-chemical luminescence(ECL) technique was used for reference to accomplish color develop-ment. You get an impression that the authors don t have a clue.  ,
Ag(I) camphorimine complexes with antimicrobial activity towards clinically important bacteria and species of the Candida genus
Authors: Marta M Alves
M F√°tima Montemor
Nuno P Mira
Jorge H Leit√£o
Jo√£o M S Cardoso
M Fernanda N N Carvalho
Andreia Louren√ßo
Soraia I Guerreiro
Journal: PLoS ONE (2017)
Discipline: Multidisciplinary
Keywords: silver camphorimine complexes; antibacterial activity; antifungal activity; Staphylococcus aureus; Pseudomonas aeruginosa
Affiliations: Centro de Qu√≠mica Estrutural, Instituto Superior T√©cnico, Universidade de Lisboa, Av. Rovisco Pais Lisboa, Portugal., iBB-Institute for Bioengineering and Biosciences and Department of Bioengineering, Instituto Superior T√©cnico, Universidade de Lisboa, Av. Rovisco Pais, Lisboa, Portugal.

Abstract:  The present work follows a previous report describing the antibacterial activity of silver camphorimine complexes of general formula [Ag(NO3)L]. The synthesis and demonstration of the antifungal and antibacterial activity of three novel [Ag(NO3)L] complexes (named 1, 2 and 3) is herein demonstrated. This work also shows for the first time that the previously studied complexes (named 4 to 8) also exert antifungal activity. The antibacterial activity of complexes was evaluated against Staphylococcus aureus, Pseudomonas aeruginosa, Burkholderia contaminans and Escherichia coli strains, while antifungal activity was tested against the Candida species C. albicans, C. glabrata, C. parapsilosis and C. tropicalis. The antimicrobial activity of the complexes ranged from very high (complex 4) to moderate (complex 6) or low (complex 8), depending on the structural and electronic characteristics of the camphorimine ligands. Notably, the highest antibacterial and anti-Candida activities do not coincide in the same complex and in some cases they were even opposite, as is the case of complex 4 which exhibits a high anti-bacterial and low antifungal activity. These distinct results suggest that the complexes may have different mechanisms against prokaryotic and eukaryotic cells. The antifungal activity of the Ag(I) camphorimine complexes (in particular of complex 1) was found to be very high (MIC = 2 Œºg/mL) against C. parapsilosis, being also registered a prominent activity against C. tropicalis and C. glabrata. None of the tested compounds inhibited C. albicans growth, being this attributed to the ability of these yeast cells to mediate the formation of less toxic Ag nanoparticles, as confirmed by Scanning Electron Microscopy images. The high antibacterial and anti-Candida activities of the here studied camphorimine complexes, especially of complexes 1 and 7, suggests a potential therapeutic application for these compounds. 

Retracted: No

PubPeer comments:
 In figure 4 A, none of the magnified boxes (labelled 1 , 2 , and 2 by me) show what is comprised in the dashed lines in the panels 1 and 2. The figure legend is very brief - are the boxes not to represent a higher magnification of the boxed areas in the larger panels? Could the authors clarify?  ,
R-flurbiprofen reverses multidrug resistance, proliferation and metastasis in gastric cancer cells by p75(NTR) induction
Authors: Li Sun
Lili Liu
Liucun Gao
Qiong Wu
Yanglin Pan
Na Liu
Haifeng Jin
Kaichun Wu
Hai Shi
Xiaohua Li
Zhiping Yang
Zhipeng Wang
Hongxi Zhao
Liu Hong
Daiming Fan
Jie Liang
Journal: Molecular Pharmaceutics (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: NSAIDs; Cox-2 inhibition; R-flurbiprofen; gastric cancer cells; proliferation
Affiliations: State Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, Department of Pharmacology, School of Pharmacy, the Fourth Military Medical University, and Department of Gynecology and Obstetrics, Tangdu Hospital, the Fourth Military Medical University

Abstract:  Nonsteroidal anti-inflammatory drugs (NSAIDs) can inhibit cell growth and metastasis, and induce cell apoptosis in cancerous cells. They have been shown to reduce incidence and mortality of gastric cancer by an unknown mechanism. NSAIDs often exert their effects by Cox-2 inhibition, and Cox-2 is overexpressed in gastric cancer cells. Nevertheless, when gastric cancer cells were treated with different NSAIDs, the non-Cox-2-inhibiting R-flurbiprofen was most effective at reducing proliferation of gastric cancer cells in vitro. R-Flurbiprofen prevented the metastatic characteristics of gastric cancer cells in vitro, and reduced tumor size and metastasis in vitro, when gastric cancer cells were injected into nude mice. R-Flurbiprofen also affected multidrug resistance, increasing the sensitivity of resistant gastric cancer cells to chemotherapeutic agents. Mechanistically, R-flurbiprofen was found to have pleiotropic effects, changing levels of cell cycle factors like Cyclin D1 and CKD4, apoptotic protwins like caspase3 and Bcl-2, and protwins that affect metastasis, like metalloproteases. Consistent with reports on other cancer cell types, NSAID treatment with R-flurbiprofen increased levels of the tumor suppressor neurotrophin receptor (p75(NTR)) in gastric cancer cells. The anticancer effects of R-flurbiprofen were found to require induction of p75(NTR) via the p38 signaling pathway, suggesting a possible mechanism of action. 

Retracted: No

PubPeer comments:
   ,
Analysis on the alterations of lens proteins by Vitex negundo in selenite cataract models
Authors: Annie Abraham
B N Rooban
V Sahasranamam
V Sasikala
Journal: Molecular vision (2011)
Discipline: CLINICAL MEDICINE
Keywords: Cataract; oxidative damage; protein modification; proteomic; microscopic
Affiliations: Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, India.

Abstract:  Purpose: Cataract is the leading cause of blindness and is associated with oxidative damage and protein modification in the lens. In the present study, we have employed proteomic and microscopic approaches to investigate the attenuation of selenite cataract by the flavonoids from Vitex negundo (FVN). Methods: To demonstrate this attenuation, Sprague-Dawley rat pups were divided into control (G I), selenite induced (G II), and selenite + FVN treated (G III). Cataract was induced by single subcutaneous injection of sodium selenite (4 mg/Kg bodyweight) on the 10th day and FVN (1 mg/Kg bodyweight) administered intraperitoneally from the 8th to the 15th day. Results: Our study indicated that chaperone property of Œ±-crystallin and soluble protein levels were reduced in the selenite induced group. Post translational modifications identified by two dimensional-polyacrylamide gel electrophoresis (2D-PAGE) and immunoblot analysis revealed the loss of cytoskeletal proteins in selenite induced group. Damage of lenticular membrane and abnormal fiber structure were observed by electron microscopy. Conclusions: The results of this study suggest that FVN modulated selenite induced cataractogensis in rat pups by preventing loss of chaperone property, various changes in lens proteins, and lens structure, further strengthening its protective role. 

Retracted: No

PubPeer comments:
 Figure 6A. * Boxes of the same color focus attention to areas within the same photo that are unexpectedly similar.  ,
The fragile X syndrome protein represses activity-dependent translation through CYFIP1, a new 4E-BP
Authors: Nahum Sonenberg
Mauro Costa-Mattioli
Valentina Mercaldo
Francesca Zalfa
Claudia Bagni
Boris Eleuteri
Daniele Di Marino
Evita Mohr
Pietro Pilo Boyl
Silvia De Rubeis
Tilmann Achsel
Walter Witke
Ilaria Napoli
Marzia Massimi
Mattia Falconi
Journal: Cell (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: mRNA translation; synaptic plasticity; brain development; FMRP; CYFIP1/Sra1
Affiliations: Department of Biology, University Tor Vergata, Rome, Italy.

Abstract:  Strong evidence indicates that regulated mRNA translation in neuronal dendrites underlies synaptic plasticity and brain development. The fragile X mental retardation protein (FMRP) is involved in this process; here, we show that it acts by inhibiting translation initiation. A binding partner of FMRP, CYFIP1/Sra1, directly binds the translation initiation factor eIF4E through a domain that is structurally related to those present in 4E-BP translational inhibitors. Brain cytoplasmic RNA 1 (BC1), another FMRP binding partner, increases the affinity of FMRP for the CYFIP1-eIF4E complex in the brain. Levels of proteins encoded by known FMRP target mRNAs are increased upon reduction of CYFIP1 in neurons. Translational repression is regulated in an activity-dependent manner because BDNF or DHPG stimulation of neurons causes CYFIP1 to dissociate from eIF4E at synapses, thereby resulting in protein synthesis. Thus, the translational repression activity of FMRP in the brain is mediated, at least in part, by CYFIP1. 

Retracted: No

PubPeer comments:
 Figure 1C. https: imgur.com GU7GrkB ,
Calorie restriction prevents the development of insulin resistance and impaired lipid metabolism in gestational diabetes offspring
Authors: Qiu-Wei Wang
Tao Li
Long Chen
Li-Ping Huang
Gang Liu
Keyang Chen
Li-Juan Hou
Chuan-Lai Hu
Journal: Pediatric Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Gestational diabetes mellitus; Calorie restriction; Offspring; Insulin resistance; Obesity
Affiliations: Department of Nutrition and Food Safety, Anhui Medical University School of Public Health, Anhui, China., Department of Public Health Inspection and Quarantine Science, Anhui Medical University, Anhui, China.

Abstract:  Background: Gestational diabetes mellitus (GDM) has long-lasting influence on offspring, which is associated with increased risks of insulin resistance, obesity, and type II diabetes mellitus. Calorie restriction (CR) is one of the most common and available nutritional interventions to prevent obesity and diabetes. We are trying to explore the effect of CR on GDM offspring. Methods: The streptozotocin was used to stimulate C57BL/6J mice to develop GDM, a number of metabolic characteristics and related protein expressions were determined in GDM offspring that were fed ad-libitum or treated with calorie restriction. Results: CR reduced body weight and glucose levels in GDM offspring. CR modulated the lipid metabolism by decreasing triglyceride and cholesterol levels in plasma. We also found that the effect of CR on insulin sensitivity may involve in signaling pathway through the regulations of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and protein kinase B (Akt). Conclusion: GDM is a high risk factor for GDM offspring to develop insulin resistance, while CR could ameliorate this adverse outcome. Moreover, the specific decrease in PTEN activation and increase in Akt phosphorylation in livers of GDM offspring with CR improved insulin sensitivity and lipid metabolism. 

Retracted: No

PubPeer comments:
  , 
 Same GAPDH blot in Figures 5 and 6. ,
Makorin-2 is a neurogenesis inhibitor downstream of phosphatidylinositol 3-kinase/Akt (PI3K/Akt) signal
Authors: William K C Cheung
Guo-Qing Wu
Pai-Hao Yang
Zhu Chen
Hsiang-Fu Kung
Marie C M Lin
Qiu-Hua Huang
Ming-Liang He
Ying Peng
Bing-Hua Jiang
Dan Xie
Journal: Journal of Biological Chemistry (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Makorin-2; Xenopus; neurogenesis; dorso-posterior deficiencies; small-head/short-tail phenotype
Affiliations: Joint State Key Laboratory in Oncology in South China, Sun Yat-Sen University, Guangzhou, China.

Abstract:  Makorin-2 belongs to the makorin RING zinc finger gene family, which encodes putative ribonucleoproteins. Here we cloned the Xenopus makorin-2 (mkrn2) and characterized its function in Xenopus neurogenesis. Forced overexpression of mkrn2 produced tadpoles with dorso-posterior deficiencies and small-head/short-tail phenotype, whereas knockdown of mkrn2 by morpholino antisense oligonucleotides induced double axis in tadpoles. In Xenopus animal cap explant assay, mkrn2 inhibited activin, and retinoic acid induced animal cap neuralization, as evident from the suppression of a pan neural marker, neural cell adhesion molecule. Surprisingly, the anti-neurogenic activity of mkrn2 is independent of the two major neurogenesis signaling cascades, BMP-4 and Wnt8 pathways. Instead, mkrn2 works specifically through the phosphatidylinositol 3-kinase (PI3K) and Akt-mediated neurogenesis pathway. Overexpression of mkrn2 completely abrogated constitutively active PI3K- and Akt-induced, but not dominant negative glycogen synthase kinase-3beta (GSK-3beta)-induced, neural cell adhesion molecule expression, indicating that mkrn2 acts downstream of PI3K and Akt and upstream of GSK-3beta. Moreover, mkrn2 up-regulated the mRNA and protein levels of GSK-3beta. These results revealed for the first time the important role of mkrn2 as a new player in PI3K/Akt-mediated neurogenesis during Xenopus embryonic development. 

Retracted: No

PubPeer comments:
 Fig. 5A and Fig. 5B. More similar than expected.  , 
 Fig. 4A and Fig. 4B. More similar than expected.  ,