PReD-Bench/PRed-Bench huggingface dataset:
Dietary NaCl affects bleomycin-induced lung fibrosis in mice
Authors: Wensheng Chen
Richard H Gomer
Darrell Pilling
Journal: Experimental Lung Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: NaCl; fibrocytes; inflammation; pulmonary fibrosis; salt.
Affiliations: Department of Biology, Texas A&M University, College Station, TX, USA, Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei, China

Abstract:  Purpose: High levels of NaCl in the diet are associated with both cardiac and renal fibrosis, but whether salt intake affects pulmonary fibrosis has not been examined. Aim of the study: To test the hypothesis that salt intake might affect pulmonary fibrosis. Materials and methods: Mice were fed low, normal, or high salt diets for 2 weeks, and then treated with oropharyngeal bleomycin to induce pulmonary fibrosis, or oropharyngeal saline as a control. Results: As determined by collagen staining of lung sections, and protein levels and cell numbers in the bronchoalveolar lavage (BAL) fluid at 21 days after bleomycin, the high salt diet did not exacerbate bleomycin-induced fibrosis, while the low salt diet attenuated fibrosis. For the bleomycin-treated mice, staining of the post-BAL lung sections indicated that compared to the regular salt diet, high salt increased the number of Ly6c-positive macrophages and decreased the number of CD11c and CD206-positive macrophages and dendritic cells. The low salt diet caused bleomycin-induced leukocyte numbers to be similar to control saline-treated mice, but reduced numbers of CD45/collagen-VI positive fibrocytes. In the saline controls, low dietary salt decreased CD11b and CD11c positive cells in lung sections, and high dietary salt increased fibrocytes. Conclusions: Together, these data suggest the possibility that a low salt diet might attenuate pulmonary fibrosis. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have two images which overlap (red boxes), suggesting that they did not come from differently treated mice, as described. *** ![file] *** Funding. This work was supported by NIH R01 HL118507. , 
 Thank you for catching this, we used the wrong figure in one panel. The erratum has been published as PMID: 35291890 DOI: 10.1080 01902148.2022.2050526 ,
Ni–citric acid coordination polymer as a practical catalyst for multicomponent reactions
Authors: Mohsen Nikoorazm
Bahman Tahmasbi
Arash Ghorbani-Choghamarani
Reza Azadbakht
Mostafa Koolivand
Journal: Scientific Reports (2021)
Discipline: Multidisciplinary
Keywords: Coordinative polymers; Metal-organic frameworks; Catalysis; Nickel; Citric acid

Abstract:  Coordinative polymers (CP) are a subclass of Metal-organic frameworks (MOFs) with porous microstructures which have been widely synthesized in recent years and applied in various fields especially in catalysis science. In this work Coordinative polymers (CP) of nickel and citric acid (CA) was prepared as a new catalyst (Ni-CP) and applied in organic multicomponent reactions. The obtained catalyst was characterized by SEM, WDX, EDS, AAS, FT-IR, XRD and BET analysis. N2 adsorption-desorption isotherms indicate good BET surface area for Ni-CP; therefore can be employed as an efficient catalyst in multicomponent reactions for the synthesis of polyhydroquinoline and 2,3-dihydroquinazolin-4(1H)-one derivatives. Finally, this catalyst was recovered and reused several consecutive times. 

Retracted: No

PubPeer comments:
 In Figure 10 the bars have all the same height although the yields are different. Also yield is spelled wrong. ,
Tumor-derived mutations in the gene associated with retinoid interferon-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3) activity and promote oncogenesis
Authors: Sudhakar Kalakonda
Robert R Lorenz
Daniel J Lindner
Shreeram C Nallar
Xiao Weihua
Dhananjaya V Kalvakolanu
Eric Lamarre
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: STAT3; GRIM-19; mutations; apoptosis; proliferation
Affiliations: Department of Microbiology and Immunology, Program in Oncology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201., Taussig Cancer Center, Cleveland Clinic Foundation, Cleveland, Ohio 44195., Head and Neck Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195., University of Science Technology, 230027 Hefei, China., Department of Microbiology and Immunology, Program in Oncology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201. Electronic address: .

Abstract:  The signal transducer and activator of transcription 3 (STAT3) protein is critical for multiple cytokine and growth factor-induced biological responses in vivo. Its transcriptional activity is controlled by a transient phosphorylation of a critical tyrosine. Constitutive activation of STAT3 imparts resistance to apoptosis, promotes cell proliferation, and induces de novo micro-angiogenesis, three of the six cardinal hallmarks of a typical cancer cell. Earlier we reported the isolation of GRIM-19 as a growth suppressor using a genome-wide expression knockdown strategy. GRIM-19 binds to STAT3 and suppresses its transcriptional activity. To understand the pathological relevance of GRIM-19, we screened a set of primary head and neck tumors and identified three somatic mutations in GRIM-19. Wild-type GRIM-19 suppressed cellular transformation by a constitutively active form of STAT3, whereas tumor-derived mutants L71P, L91P and A95T significantly lost their ability to associate with STAT3, block gene expression, and suppress cellular transformation and tumor growth in vivo. Additionally, these mutants lost their capacity to prevent metastasis. These mutations define a mechanism by which STAT3 activity is deregulated in certain human head and neck tumors. 

Retracted: No

PubPeer comments:
 Could the authors please check the labeling for the Actin bands in Figure 3D and Figure 8C. The bands appear the same, but the lanes seem to be labeled differently. *** ![file] , 
 #1 The same thing appears to be true for the Actin bands in Figure 2B and Figure 9C. Apologies if I m misunderstanding something. ,
Tbx3 is a downstream target of the Wnt/beta-catenin pathway and a critical mediator of beta-catenin survival functions in liver cancer
Authors: Christine Perret
Marie-Annick Buendia
Charlotte Labalette
Aurélien de Reyniès
Stefano Cairo
Pascal Pineau
Christine Neuveut
Carolina Armengol
Delphine Cougot
Claire-Angélique Renard
Yu Wei
Anne Dejean
Journal: Cancer Research (2007)
Discipline: CLINICAL MEDICINE
Keywords: Tbx3; transcriptional repressor; Wnt/beta-catenin; liver tumorigenesis; mutation
Affiliations: Institut National de la Sante et de la Recherche Medicale U579, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris, France.

Abstract:  Tbx3 encodes a transcriptional repressor that is important for diverse patterning events during development, and Tbx3 mutation in humans causes the ulnar-mammary syndrome. Here, we describe the identification of Tbx3 in array-based search for genes downstream Wnt/beta-catenin that are implicated in liver tumorigenesis. Overexpression of Tbx3 is closely associated with the mutational status of beta-catenin in murine liver tumors induced by Myc as well as in human hepatocellular carcinomas and hepatoblastomas. Moreover, Tbx3 transcription is activated by ectopic expression of beta-catenin in mouse liver and in human tumor cell lines. Evidence that Tbx3 transcription is directly regulated by beta-catenin is provided by chromatin immunoprecipitation and reporter assays. Although HepG2 cells stably transfected with Tbx3 display moderately enhanced growth rate, the dominant negative mutant Tbx3-Y149S drastically inhibits hepatoma cell growth in vitro and in vivo. Moreover, small interfering RNAs (siRNA) directed against Tbx3 inhibit anchorage-independent growth of liver and colon carcinoma cells. We further show that inhibition of Tbx3 expression by specific siRNAs blocks beta-catenin-mediated cell survival and renders cells sensitive to doxorubicin-induced apoptosis. Conversely, ectopic expression of Tbx3 inhibits apoptosis induced by beta-catenin depletion. Marked overexpression of Tbx3 in a subset of hepatoblastomas is associated with chemotherapy-resistant phenotype and unfavorable patient outcome. These results reveal an unsuspected role of Tbx3 as a mediator of beta-catenin activities on cell proliferation and survival and as an important player in liver tumorigenesis. 

Retracted: No

PubPeer comments:
null, 
 Figures 1A and 1B. ![] , 
 An apparent image duplication in figure 5 as well (see below): ![file] ,
Carcinoma associated fibroblasts small extracellular vesicles with low miR-7641 promotes breast cancer stemness and glycolysis by HIF-1α
Authors: Yanxia Zhan
Fanli Hua
Yonglei Liu
Jianfang Xie
Yanfei Yang
Yunfeng Cheng
Feng Li
Journal: Cell Death Discovery (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Fibroblasts; cancer development; progression; small extracellular vesicles (sEVs); cancer-associated fibroblasts

Abstract:  Fibroblasts play an important role in cancer development and progression. Small extracellular vesicles (sEVs) are one type of extracellular vesicles, which mediate the interaction between cancer-associated fibroblasts and cancer cells by transferring their contents. However, the roles of sEVs from cancer-associated fibroblasts on breast cancer stem cell properties are largely unraveled. The purpose of this study was to explore the roles of sEVs from cancer-associated fibroblasts on breast cancer progression. The miRNA array data showed a different miRNA profile between CAFs sEVs and normal fibroblasts sEVs. By verification using real-time RT-PCR, the data analysis indicated that miR-7641 levels were lower in sEVs from CAFs compared with NFs. The cellular functions were assayed and the results indicated that CAFs derived sEVs with low miR-7641 levels suppressed breast cancer cell survival, glycolysis, and stem cell properties via the HIF-1α pathway. Collectively, these findings indicated that sEVs from CAFs promoted breast cancer stem cell properties and glycolysis via miR-7641/HIF-1α, which was a possible new way for targeting breast cancer. 

Retracted: No

PubPeer comments:
 Clearly same image has been used twice for different experimental conditions as shown below (Fig 5A). ![file] , 
 Thanks a lot for pointing our our mistake. Following your suggestion we had written corrigendum and sent to Editor in Chief Galons Herve on 21 May 2018 for which we have not received any reply from him. Content goes as follows Dear Prof. Galons This is with regards to our earlier accepted manuscript,  Aegeline inspired synthesis of novel amino alcohol and thiazolidinedione hybrids with antiadipogenic activity in 3T3-L1 cells which appeared in European Journal of Medicinal Chemistry 143 (2018) 780e791. One of the representative images in Fig. 5A in 0-2 days has been inadvertently pasted for 0-4 day also. It is a copy and paste error during image processing; however, the change in representative image does not affect the quantification data in Fig 5B. The conclusion of the findings in the paper remains unaltered. Below are the old and new images with the change highlighted. I apologize for the inconvenience caused by this error. I request you to publish a corrigendum in this regard in the recent upcoming issue. Thanking you, Sincerely Anil Gaikwad P. S. I am unable to see image in preview although I am uploading file 71 KB. Kindly suggest for image uploading , 
 ![file] ,
MicroRNA-139 inhibits hepatocellular carcinoma cell growth through down-regulating karyopherin alpha 2
Authors: Lei Dong
Liang Liang
Zhijun Dai
Ying Zan
Tian Tian
Yujiao Deng
Baofeng Wang
Journal: Journal of Experimental & Clinical Cancer Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: Colony formation; Epithelial-to-mesenchymal transition; Migration and invasion; Survival.
Affiliations: Department of Oncology, the Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, 710004, China., Department of Oncology, the Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, 710004, China. ., Department of Gastroenterology, the Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, 710004, China. .

Abstract:  Background: MicroRNA-139-5p (miR-139) has been shown to play important roles in hepatocellular carcinoma (HCC) development. However, the exact mechanism of miR-139 in HCC remains largely unknown. Methods: We investigated the function in human cell lines and patient tissue samples by experimental techniques in molecular biology including Co-IP assay, cell viability assay, quantitative real-time-PCR, et al. In addition, datasets were used to verify the results by database analysis. Statistical analysis was performed by using the GraphPad Prism 6 (GraphPad Software Inc., USA). A P value &lt; 0.05 was defined as statistically significant. Results: In this study, we found that miR-139 was significantly down-regulated in HCC. MiR-139 level was negatively associated with the stage of HCC, and HCC patients with higher miR-139 level had longer overall survival (OS) than these having lower miR-139 expression. Overexpression of miR-139 led to reduced cell viability, elevated apoptosis, and decreased colony forming, migratory and invasive capacities in HCC cells, while down-regulation of miR-139 led to opposite phenotypes. MiR-139 also inhibited HCC growth in a xenograft mouse model. We identified karyopherin alpha 2 (KPNA2) as a direct target of miR-139. KPNA2 is up-regulated in HCC and higher KPNA2 level is associated with poor patient prognosis. Silencing of KPNA2 expression led to similar phenotypic changes as miR-139 overexpression. Restoration of KPNA2 attenuated the suppressive effects of miR-139 overexpression on cell viability, apoptosis, colony formation, migration and invasion. In addition, miR-139 overexpression and KPNA2 depletion led to decreased nucleus level of POU class 5 homeobox 1 (POU5F1) and c-myc, two well-known pro-oncogenes. Conclusion: In together, these data revealed the essential roles of the miR-139/KPNA2 axis in HCC. 

Retracted: No

PubPeer comments:
 Figure 7F. * Red boxes: Two panels appear to show an area of overlap. ![file] ,
Feasibility between Bifidobacteria Targeting and Changes in the Acoustic Environment of tumor Tissue for Synergistic HIFU
Authors: Huanan Li
Jie Xiong
Hai Qiao
Jianzhong Zou
Wenjuan Zou
Binglei Jiang
Chun Chen
Yong Luo
Yaotai Wang
Die Xu
Yu Tang
Xuan Gao
Fujie Jiang
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: High intensity focused ultrasound (HIFU); AET; Bifidobacterium longum; tumor tissues; collagen fibres
Affiliations: State Key Laboratory of Ultrasound Engineering in Medicine Co-Founded by Chongqing and the Ministry of Science and Technology, Chongqing Collaborative Innovation Center for Minimally-invasive and Noninvasive Medicine, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China., Chongqing Traditional Chinese Medicine Hospital, Chongqing, 400021, China., State Key Laboratory of Ultrasound Engineering in Medicine Co-Founded by Chongqing and the Ministry of Science and Technology, Chongqing Collaborative Innovation Center for Minimally-invasive and Noninvasive Medicine, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China. .

Abstract:  High intensity focused ultrasound (HIFU) has been recently shown as a rapidly developing new technique for non-invasive ablation of local tumors whose therapeutic efficiency can be significantly improved by changing the tissue acoustic environment (AET). Currently, the method of changing AET is mainly to introduce a medium with high acoustic impedance, but there are some disadvantages such as low retention of the introduced medium in the target area and a short residence time during the process. In our strategy, anaerobic bacterium Bifidobacterium longum (B. longum) which can colonize selectively in hypoxic regions of the animal body was successfully localized and shown to proliferate in the hypoxic zone of tumor tissue, overcoming the above disadvantages. This study aimed to explore the effects of Bifidobacteria on AET (including the structure and acoustic properties of tumor tissues) and HIFU ablation at different time. The results show that the injection of Bifidobacteria increased the collagen fibre number, elastic modulus and sound velocity and decreased neovascularization in tumor tissues. The number of collagen fibres and neovascularization decreased significantly over time. Under the same HIFU irradiation intensity, the B. longum injection increased the coagulative necrosis volume and decreased the energy efficiency factor (EEF). This study confirmed that Bifidobacteria can change the AET and increase the deposition of ultrasonic energy and thereby the efficiency of HIFU. In addition, the time that Bifidobacteria stay in the tumor area after injection is an important factor. This research provides a novel approach for synergistic biologically targeted HIFU therapy. 

Retracted: No

PubPeer comments:
 Image duplication (between treated and control!) in Figure 1: Heart detail: ![file] Lung detail: ![file] Overview: , 
 My screenshot for the figure overview accidentally included the volume-change icon! Here is a better screenshot: ![file] ,
FLIP protects against hypoxia/reoxygenation-induced endothelial cell apoptosis by inhibiting Bax activation
Authors: Hong Pyo Kim
Augustine M K Choi
Yong Wang
Jinglan Zhang
Xue Wang
Stefan W Ryter
Journal: Molecular and Cellular Biology (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Hypoxia/reoxygenation; cell death; regulatory mechanisms; death receptor; mitochondria-dependent
Affiliations: Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, 3459 Fifth Ave., MUH NW 628, Pittsburgh, PA 15213, USA.

Abstract:  Hypoxia/reoxygenation causes cell death, yet the underlying regulatory mechanisms remain partially understood. Recent studies demonstrate that hypoxia/reoxygenation can activate death receptor and mitochondria-dependent apoptotic pathways, involving Bid and Bax mitochondrial translocation and cytochrome c release. Using mouse lung endothelial cells (MLEC), we examined the role of FLIP, an inhibitor of caspase 8, in hypoxia/reoxygenation-induced cell death. FLIP protected MLEC against hypoxia/reoxygenation by blocking both caspase 8/Bid and Bax/mitochondrial apoptotic pathways. FLIP inhibited Bax activation in wild-type and Bid(-/-) MLEC, indicating independence from the caspase 8/Bid pathway. FLIP also inhibited the expression and activation of protein kinase C (PKC) (alpha, zeta) during hypoxia/reoxygenation and promoted an association of inactive forms of PKC with Bax. Surprisingly, FLIP expression also inhibited death-inducing signal complex (DISC) formation in the plasma membrane and promoted the accumulation of the DISC in the Golgi apparatus. FLIP expression also upregulated Bcl-X(L), an antiapoptotic protein. In conclusion, FLIP decreased DISC formation in the plasma membrane by blocking its translocation from the Golgi apparatus and inhibited Bax activation through a novel PKC-dependent mechanism. The inhibitory effects of FLIP on Bax activation and plasma membrane DISC formation may play significant roles in protecting endothelial cells from the lethal effects of hypoxia/reoxygenation. 

Retracted: No

PubPeer comments:
 This acticle has been corrected. The correction notice reads: We noticed an error in Figure 4G, where the HE (200 x) for shROR1+Twist was misplaced with the same HE picture for Twist. The figure with the error corrected is shown below. The correction made in this erratum does not affect the original conclusions or any part of the text and figure legends. The authors wish to apologize for any inconvenience or misunderstanding that this error may have caused. https: www.thno.org v11p2077.htm#coraddress ,
TLX activates MMP-2, promotes self-renewal of tumor spheres in neuroblastoma and correlates with poor patient survival
Authors: S Mohlin
K Funa
E Johansson
P L Chavali
A Hayashi
D R Kaplan
D Vizlin-Hodzic
S Påhlman
L Hansford
Q Zhai
Z-j Zeng
S Venkatabalasubramanian
R K R Saini
Journal: Cell death & disease (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Nuclear orphan receptor TLX; neuroblastoma; tumor spheres; neural stem/progenitor cells; self-renewal
Affiliations: 1] Sahlgrenska Cancer Center at the Sahlgrenska Academy, University of Gothenburg, Box 425, Gothenburg SE 40530, Sweden [2] Department of Oncology, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK., Sahlgrenska Cancer Center at the Sahlgrenska Academy, University of Gothenburg, Box 425, Gothenburg SE 40530, Sweden., 1] Sahlgrenska Cancer Center at the Sahlgrenska Academy, University of Gothenburg, Box 425, Gothenburg SE 40530, Sweden [2] School of Chemical and Biotechnology, SASTRA University, Thanjavur 613401, India., 1] Sahlgrenska Cancer Center at the Sahlgrenska Academy, University of Gothenburg, Box 425, Gothenburg SE 40530, Sweden [2] Molecular Biology Research Center, School of Biological Science and Technology, Central South University, Changsha, China., Center for Molecular Pathology, Lund University, Skåne University Hospital, Malmö SE 20502, Sweden., 1] Program in Cell Biology, Hospital for Sick Children, Toronto, Canada M5G 1X8 [2] Department of Molecular Genetics, University of Toronto, Toronto, Canada M5S 1A8.

Abstract:  Nuclear orphan receptor TLX (Drosophila tailless homolog) is essential for the maintenance of neural stem/progenitor cell self-renewal, but its role in neuroblastoma (NB) is not well understood. Here, we show that TLX is essential for the formation of tumor spheres in three different NB cell lines, when grown in neural stem cell media. We demonstrate that the knock down of TLX in IMR-32 cells diminishes its tumor sphere-forming capacity. In tumor spheres, TLX is coexpressed with the neural progenitor markers Nestin, CD133 and Oct-4. In addition, TLX is coexpressed with the migratory neural progenitor markers CD15 and matrix metalloproteinase-2 (MMP-2) in xenografts of primary NB cells from patients. Subsequently, we show the effect of TLX on the proliferative, invasive and migratory properties of IMR-32 cells. We attribute this to the recruitment of TLX to both MMP-2 and Oct-4 gene promoters, which resulted in the respective gene activation. In support of our findings, we found that TLX expression was high in NB patient tissues when compared with normal peripheral nervous system tissues. Further, the Kaplan-Meier estimator indicated a negative correlation between TLX expression and survival in 88 NB patients. Therefore, our results point at TLX being a crucial player in progression of NB, by promoting self-renewal of NB tumor-initiating cells and altering their migratory and invasive properties. 

Retracted: No

PubPeer comments:
 ![file] ![file] ,
Δ9-THC-caused synaptic and memory impairments are mediated through COX-2 signaling
Authors: Hongwei Yang
Rongqing Chen
Jian Zhang
Yan Wu
Ya-Ping Tang
Hao Sun
Zhao-Qian Teng
Yunping Song
Chu Chen
Ni Fan
Journal: Cell (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Marijuana; Δ(9)-tetrahydrocannabinol; COX-2; CB1 receptor; G protein βγ subunits
Affiliations: Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA., Department of Cell Biology and Anatomy, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA., Department of Otorhinolaryngology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.

Abstract:  Marijuana has been used for thousands of years as a treatment for medical conditions. However, untoward side effects limit its medical value. Here, we show that synaptic and cognitive impairments following repeated exposure to Δ(9)-tetrahydrocannabinol (Δ(9)-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids in the brain. COX-2 induction by Δ(9)-THC is mediated via CB1 receptor-coupled G protein βγ subunits. Pharmacological or genetic inhibition of COX-2 blocks downregulation and internalization of glutamate receptor subunits and alterations of the dendritic spine density of hippocampal neurons induced by repeated Δ(9)-THC exposures. Ablation of COX-2 also eliminates Δ(9)-THC-impaired hippocampal long-term synaptic plasticity, working, and fear memories. Importantly, the beneficial effects of decreasing β-amyloid plaques and neurodegeneration by Δ(9)-THC in Alzheimer's disease animals are retained in the presence of COX-2 inhibition. These results suggest that the applicability of medical marijuana would be broadened by concurrent inhibition of COX-2. 

Retracted: No

PubPeer comments:
 ![file] ![file] ,
WNT-LRP5 signaling induces Warburg effect through mTORC2 activation during osteoblast differentiation
Authors: Adewole L Okunade
Courtney M Karner
Bruce W Patterson
Emel Esen
Jianquan Chen
Fanxin Long
Journal: Cell Metabolism (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: WNT signaling; cell differentiation; cellular metabolism; osteoblast differentiation; Warburg effect
Affiliations: Department of Medicine, Washington University School of Medicine, Saint Louis, MO 63110, USA.

Abstract:  WNT signaling controls many biological processes including cell differentiation in metazoans. However, how WNT reprograms cell identity is not well understood. We have investigated the potential role of cellular metabolism in WNT-induced osteoblast differentiation. WNT3A induces aerobic glycolysis known as Warburg effect by increasing the level of key glycolytic enzymes. The metabolic regulation requires LRP5 but not β-catenin and is mediated by mTORC2-AKT signaling downstream of RAC1. Suppressing WNT3A-induced metabolic enzymes impairs osteoblast differentiation in vitro. Deletion of Lrp5 in the mouse, which decreases postnatal bone mass, reduces mTORC2 activity and glycolytic enzymes in bone cells and lowers serum lactate levels. Conversely, mice expressing a mutant Lrp5 that causes high bone mass exhibit increased glycolysis in bone. Thus, WNT-LRP5 signaling promotes bone formation in part through direct reprogramming of glucose metabolism. Moreover, regulation of cellular metabolism may represent a general mechanism contributing to the wide-ranging functions of WNT proteins. 

Retracted: No

PubPeer comments:
 Is S6 blot just a longer exposure of beta-actin? ![file] , 
 #1 Thanks for identifying the error. We have now corrected the S6 blot. Duplicate gels were run in this experiment and both membranes were used for detection of the various proteins and phospho-proteins. Unfortunately a mistake was made during compilation of the figure. A corrected version of the figure is posted here. We apologize for the error. -Emel Esen and Fanxin Long ![file] ,
The involvement of AQP1 in myocardial edema induced by pressure overload in mice
Authors: D-S Sang
Y-J Li
D Song
Y Yang
X Tian
N He
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Aquaporin-1; heart edema; transverse aortic constriction; myocardial edema; cardiac function
Affiliations: Department of Cardiology, Hebei Medical University, Shijiazhuang, China. .

Abstract:  Objective: To investigate the effect of aquaporin-1 (AQP1) on heart edema induced by transverse aortic constriction (TAC) in mice, and to explore whether inhibiting the expression of AQP1 could attenuate myocardial edema and improve cardiac function. Materials and methods: The C57BL/6 mice were divided into four groups: (1) the sham group; 2) the sham + acetazolamide group: mice were orally gavaged with acetazolamide (20 mg/kg/day) after sham operation; (3) the TAC group: a mouse model of pressure overload induced by TAC for two weeks; (4) the TAC + acetazolamide group: mice were orally gavaged with acetazolamide (20 mg/kg/day) after TAC. Cardiac function was detected by echocardiography after 2 weeks' TAC. The ratio of heart weight to body weight (HW/BW) and myocardial water content were calculated. The mRNA and protein expressions of AQP1 were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot, respectively. Results: Significant myocardial hypertrophy and dysfunction were found in TAC mice. The ratio of HW/BW, myocardial water content, and the mRNA and protein expression of AQP1 of the TAC group were markedly higher than those of the sham group. By contrast, acetazolamide administration reduced the ratio of HW/BW and myocardial water content, whereas improved cardiac dysfunction induced by TAC. Moreover, acetazolamide reduced the mRNA and protein expression of AQP1 in TAC mice. Conclusions: The expression of AQP1 was closely related to myocardial edema induced by TAC. The inhibition of AQP1 could reduce myocardial edema and improve cardiac dysfunction. 

Retracted: No

PubPeer comments:
 Figure 1B. * Red boxes: The  sham and the  sham+ace panels appear to show an overlap. ![file] ,
Dinitrosopiperazine-mediated phosphorylated-proteins are involved in nasopharyngeal carcinoma metastasis
Authors: Gongjun Tan
Zhenlin Zhang
Yuejin Li
Chaojun Duan
Zhengke Peng
Jinping Lu
Faqing Tang
Na Liu
Xiaowei Tang
Guangrong Yan
Damao Huang
Journal: International Journal of Molecular Sciences (2014)
Discipline: CHEMISTRY
Keywords: N,N'-dinitrosopiperazine; nasopharyngeal carcinoma; metastasis; phosphoproteins; motility
Affiliations: Medical Research Center and Clinical Laboratory, Zhuhai Hospital of Jinan University, 79 Kangning Road, Zhuhai 519000, China. ., Metallurgical Science and Engineering, Central South University, 21 Lushan South Road, Changsha 410083, China. ., Clinical Laboratory and Medical Research Center, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, China. ., Institute of Life and Health Engineering, National Engineering and Research Center for Genetic Medicine, Jinan University, 601 Huangpu Road West, Guangzhou 510632, China. .

Abstract:  N,N'-dinitrosopiperazine (DNP) with organ specificity for nasopharyngeal epithelium, is involved in nasopharyngeal carcinoma (NPC) metastasis, though its mechanism is unclear. To reveal the pathogenesis of DNP-induced metastasis, immunoprecipitation was used to identify DNP-mediated phosphoproteins. DNP-mediated NPC cell line (6-10B) motility and invasion was confirmed. Twenty-six phosphoproteins were increased at least 1.5-fold following DNP exposure. Changes in the expression levels of selected phosphoproteins were verified by Western-blotting analysis. DNP treatment altered the phosphorylation of ezrin (threonine 567), vimentin (serine 55), stathmin (serine 25) and STAT3 (serine 727). Furthermore, it was shown that DNP-dependent metastasis is mediated in part through ezrin at threonine 567, as DNP-mediated metastasis was decreased when threonine 567 of ezrin was mutated. Strikingly, NPC metastatic tumors exhibited a higher expression of phosphorylated-ezrin at threonine 567 than the primary tumors. These findings provide novel insight into DNP-induced NPC metastasis and may contribute to a better understanding of the metastatic mechanisms of NPC tumors. 

Retracted: Yes

PubPeer comments:
 Figure 5. Colud the author check if they really placed Merge Images? It seems nothing from u03b3H2AX images was shown in the merge images. ![file] ,
LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer
Authors: Jibin Li
Xiaofei Yan
Rui Zhang
Zhao Jian
Su Meng
Journal: Molecular Medicine Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: lncRNAs; colorectal cancer; SNHG6; ETS1; proliferation
Affiliations: Department of Medical Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China.

Abstract:  The term 'long non‑coding RNAs' (lncRNAs) refers to all non‑protein coding transcripts &gt;200 nucleotides in length. Dysregulation of lncRNAs has been identified in colorectal cancer, which is one of the more serious types of cancer worldwide, third place in the mortality rates, and is associated with poor prognoses. Novel evidence suggests that lncRNAs serve an important role in regulating the development and progression of colorectal cancer. In the present study, it was demonstrated that SNHG6 expression was downregulated in colorectal cancer tissues by reverse transcription quantitative polymerase chain reaction assays; however, ETS1 expression levels were upregulated. Overexpression of SNHG6 not only inhibited the proliferation of colon cancer cells in vitro by inducing apoptosis, but also inhibited cell proliferation, invasion and migration. The overexpression of SNHG6 inhibited colon cell viability and proliferation by targeting ETS1 through the phosphoinositide 3‑kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. These results suggested that SNHG6 may directly suppress ETS1, which may be one of potential mechanisms through which it inhibits the viability and proliferation of colorectal cancer cells, and it provides novel insight into the carcinogenesis of colorectal cancer. In addition, it may assist in the development of a treatment approach for ETS1‑activated colorectal cancer. 

Retracted: No

PubPeer comments:
 Fig 3C.  The effect of pWPXL-SNHG6 or si-SNHG6 on the invasion of HCT-116 cells was determined using Transwell invasion assays . ![file] For comparison: Fig 3C from [Zhang et al (2018)] .  Twenty-four hours post-transfection, cell invasion was evaluated in HCT116 cells using a Transwell system with 8 u03bcm pores in polycarbonate membranes. Representative views are shown. ![file] ,
Is TCRgamma clonality assay useful to detect early celiac disease?
Authors: Gabrio Bassotti
Guido Rindi
Francesco Lanzarotto
Fabio Facchetti
Alberto Lanzini
Vincenzo Villanacci
Alessandro Ubiali
Journal: Journal of clinical gastroenterology (2007)
Discipline: CLINICAL MEDICINE
Keywords: histology; celiac disease; TCRgamma clonality assay; intraepithelial T cells; laboratory tests
Affiliations: Second Pathology Unit, Spedali Civili, Brescia, Italy.

Abstract:  Background: Although histology is considered the gold standard for the diagnosis of celiac disease, the early stages (latent or potential) of this disease are difficult to diagnose, because of the negativity of laboratory tests and the lack of villous atrophy. Thus, markers of early disease are needed. Aims: We investigated the possibility to detect latent or potential celiac disease by means of TCRgamma clonality assay in intraepithelial T cells in patients with suspected disease, negative laboratory tests, and an increased number of intraepithelial lymphocytes. Patients and methods: Duodenal biopsies were obtained from 35 patients with nonspecific duodenitis (controls), 13 latent or potential celiac disease subjects, 28 well-defined celiac patients, and 8 celiac patients in gluten-free diet. Histologic and immunohistochemical quantification of intraepithelial lymphocytes, as well as TCRgamma clonality assay, were carried out in all subjects by means of standard techniques. Results: Intraepithelial lymphocytes and TCRgamma clonality were significantly increased in potential and defined celiac patients with respect to the controls, even though the increase in TCRgamma clonality was lesser with respect to that of intraepithelial lymphocytes. No significant differences were found concerning this variable between the potential and defined celiac subjects. Conclusions: TCRgamma clonality does not represent a marker of early disease. However, it might be useful to help in distinguishing celiac disease from other causes of nonspecific duodenitis. 

Retracted: No

PubPeer comments:
 Images duplication by some of the same authors. In one paper the image refers to a pediatric population and in the other to adult patients. ![file] , 
 More duplications ![file] , 
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 The Ambassadors vs celiac histology. ![file] , 
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Lactobacillus Cell Surface Proteins Involved in Interaction with Mucus and Extracellular Matrix Components
Authors: Barbara De Siena
Rosangela Marasco
Lidia Muscariello
Journal: Current Microbiology (2020)
Discipline: MICROBIOLOGY
Keywords: gut microbiota; Lactobacilli; probiotic strains; pathogens; immune system
Affiliations: Dipartimento Di Scienze E Tecnologie Ambientali, Biologiche E Farmaceutiche, Università Degli Studi Della Campania "L. Vanvitelli", via Vivaldi 43, 81100, Caserta, Italy., Dipartimento Di Scienze E Tecnologie Ambientali, Biologiche E Farmaceutiche, Università Degli Studi Della Campania "L. Vanvitelli", via Vivaldi 43, 81100, Caserta, Italy. .

Abstract:  The gut microbiota is a complex microbial ecosystem where bacteria, through mutual interactions, cooperate in maintaining of wellbeing and health. Lactobacilli are among the most important constituents of human and animal intestinal microbiota and include many probiotic strains. Their presence ensures protection from invasion of pathogens, as well as stimulation of the immune system and protection of the intestinal flora, often exerted through the ability to interact with mucus and extracellular matrix components. The main factors responsible for mediating adhesion of pathogens and commensals to the gut are cell surface proteins that recognize host targets, as mucus layer and extracellular matrix proteins. In the last years, several adhesins have been reported to be involved in lactobacilli-host interaction often miming the same mechanism used by pathogens. 

Retracted: No

PubPeer comments:
 Several references in Table 1 which represent an important resource have gone for a toss! There is a mismatch between the reference numbers here and the actual references list. ,
Dephosphorylation of gamma H2A by Glc7/protein phosphatase 1 promotes recovery from inhibition of DNA replication
Authors: Maria Pia Longhese
Davide Mantiero
Marco Bazzi
Camilla Trovesi
Giovanna Lucchini
Journal: Molecular and Cellular Biology (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Replication fork stalling; Rad53 phosphorylation; checkpoint activation; DNA replication forks; protein phosphatase Glc7
Affiliations: Dipartimento di Biotecnologie e Bioscienze, Università degli Studi di Milano-Bicocca, Milan, Italy., Dipartimento di Biotecnologie e Bioscienze, Università degli Studi di Milano-Bicocca, 20126 Milan, Italy

Abstract:  Replication fork stalling caused by deoxynucleotide depletion triggers Rad53 phosphorylation and subsequent checkpoint activation, which in turn play a crucial role in maintaining functional DNA replication forks. How cells regulate checkpoint deactivation after inhibition of DNA replication is poorly understood. Here, we show that the budding yeast protein phosphatase Glc7/protein phosphatase 1 (PP1) promotes disappearance of phosphorylated Rad53 and recovery from replication fork stalling caused by the deoxynucleoside triphosphate (dNTP) synthesis inhibitor hydroxyurea (HU). Glc7 is also required for recovery from a double-strand break-induced checkpoint, while it is dispensable for checkpoint inactivation during methylmethane sulfonate exposure, which instead requires the protein phosphatases Pph3, Ptc2, and Ptc3. Furthermore, Glc7 counteracts in vivo histone H2A phosphorylation on serine 129 (gamma H2A) and dephosphorylates gamma H2A in vitro. Finally, the replication recovery defects of HU-treated glc7 mutants are partially rescued by Rad53 inactivation or lack of gamma H2A formation, and the latter also counteracts hyperphosphorylated Rad53 accumulation. We therefore propose that Glc7 activity promotes recovery from replication fork stalling caused by dNTP depletion and that gamma H2A dephosphorylation is a critical Glc7 function in this process. 

Retracted: No

PubPeer comments:
 Figure 1D. * Cyan arrows: The first three lanes of the  wt and  glc7-132 panels look more similar to each other than expected. Note a small irregularity under the second lane, which looks like an eye. ![file] Figure 4A. * Pink arrows: The first lane of the  wt and the first lane of the  GAL-GLC7 panels look more similar to each other than expected. ![file] Reported to the journal in September 2016. No action was taken. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
Graphene-supported Pd catalyst for highly selective hydrogenation of resorcinol to 1, 3-cyclohexanedione through giant π-conjugate interactions
Authors: Yao Yang
Yingxin Liu
Zuojun Wei
Ruofei Pan
Yaxin Hou
Journal: Scientific reports (2015)
Discipline: Multidisciplinary
Keywords: selective hydrogenation; resorcinol; 1,3-cyclohexanedione; reduced graphene oxide; Pd catalyst
Affiliations: Key Laboratory of Biomass Chemical Engineering of the Ministry of Education, College of Chemical and Biological Engineering, Zhejiang University, Hangzhou 310027, China., College of Pharmaceutical Science, Zhejiang University of Technology, Hangzhou 310032, China.

Abstract:  The selective hydrogenation of resorcinol (RES) to 1, 3-cyclohexanedione (1,3-CHD) without the addition of alkali is a big challenge. In this article, a novel reduced graphene oxide (rGO) supported Pd catalyst was prepared through co-reduction method, over which we obtained 99.9% of resorcinol conversion and 94.2% of the ever-reported highest 1,3-cyclohexanedione selectivity at 25 °C in only CH2Cl2 solvent. The excellent selectivity was contributed to the strong π-π and p-π interactions between the graphene nanosheet and the benzene ring as well as hydroxyl in RES molecule. The followed adsorption experiment and Raman analysis also showed the existence of aromatic graphite structures in rGO, which exhibited stronger adsorption towards RES than towards 1,3-CHD. 

Retracted: No

PubPeer comments:
 Figure 1 has unexpectedly similar (002) peaks with all noise.Other parts of patterns are different. ![file] ,
RETRACTED ARTICLE: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy
Authors: Wei Chen
Hongming Pan
Xiaoyun Zhou
Yinghua Xu
Weidong Han
Wei Jin
Yu Zheng
Na Kong
Fang Lou
Liu Gong
Hong Hu
Da Li
Yong Fang
Kaifeng Wang
Xiaotong Hu
Xian Wang
Xinbing Sui
Journal: Scientific Reports (2014)
Discipline: Multidisciplinary
Keywords: p53 tumor suppressor gene; autophagy; chemotherapy resistance; 5-FU treatment; HCT116 p53(-/-)
Affiliations: 1] Department of Medical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China [2] Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, China 310016 [3]., 1] Department of Medical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China [2] Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, China 310016., Department of Medical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China., Biomedical Research Center and Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, China 310016.

Abstract:  Deficiency or mutation in the p53 tumor suppressor gene commonly occurs in human cancer and can contribute to disease progression and chemotherapy resistance. Currently, although the pro-survival or pro-death effect of autophagy remains a controversial issue, increasing data seem to support the idea that autophagy facilitates cancer cell resistance to chemotherapy treatment. Here we report that 5-FU treatment causes aberrant autophagosome accumulation in HCT116 p53(-/-) and HT-29 cancer cells. Specific inhibition of autophagy by 3-MA, CQ or small interfering RNA treatment targeting Atg5 or Beclin 1 can potentiate the re-sensitization of these resistant cancer cells to 5-FU. In further analysis, we show that JNK activation and phosphorylation of Bcl-2 are key determinants in 5-FU-induced autophagy. Inhibition of JNK by the compound SP600125 or JNK siRNA suppressed autophagy and phosphorylation of c-Jun and Bcl-2 but increased 5-FU-induced apoptosis in both HCT116 p53(-/-) and HT29 cells. Taken together, our results suggest that JNK activation confers 5-FU resistance in HCT116 p53(-/-) and HT29 cells by promoting autophagy as a pro-survival effect, likely via inducing Bcl-2 phosphorylation. These results provide a promising strategy to improve the efficacy of 5-FU-based chemotherapy for colorectal cancer patients harboring a p53 gene mutation. 

Retracted: Yes

PubPeer comments:
 The GAPDH bands in Figure 3d appear quite similar (but not identical) after horizontal flip. Could the authors please provide the original uncropped scan? *** ![file] , 
 I am Fausta Fischietti and I am the first author of this paper. The bands are clearly different. As requested, please see attached the uncropped image of the GAPDH blot, that makes clear that the panels were derived from the correct portions of the blot. For presentation purposes we separated PANC-1 and MIA-Pa-Ca-2 cells on the manuscript. ![file] , 
 #2 Thank you for providing the uncropped blot. This alleviates my concern. ,
Diagnostic challenge for ovarian malignant melanoma in premenopausal women: primary or metastatic?
Authors: Mohammed Ichou
Mohamed Oukabli
Zouhour Fadoukhair
Hind M&#x27;rabti
Habiba Kadiri
Abderrahmane Albouzidi
Hassan Errihani
Ismail Essaidi
Saoussan Kharmoum
Yassir Sbitti
Journal: World Journal of Surgical Oncology (2011)
Discipline: CLINICAL MEDICINE
Keywords: ovarian metastasis; malignant melanoma; diagnosis challenge; prognosis; case report
Affiliations: Department of Medical Oncology, University Military Hospital, Rabat, Morocco. 

Abstract:  Background: In the ovary, metastatic malignant melanoma may be confused with primary malignant melanoma and presents a diagnosis challenge. Most cases are associated with disseminated diseases and poor prognosis. We present this case report of a metastatic ovarian malignant melanoma simulating primary ovarian cancer. Case report: A 45-year-old premenopausal woman was incidentally found to have an abdominal mass, 3 years after removal of a cutaneous melanoma lesion. Ultrasound and CT scan revealed left two solid masses, which were found to be an ovarian tumor at laparotomy. Left oophorectomy was performed. Histopathology and immunohistochemistry showed melanoma metastasis to the ovary. Nine months later, the patient developed epilepsy and confusion. Magnetic Resonance Imaging showed unique Wright frontal lobe lesion. She underwent stereotactic radio surgery and dacarbazine monotherapy. For months later, the patient is died from disseminate disease progression. Conclusion: Ovarian metastasis is an unusual presentation of cutaneous melanoma and the prognosis was dismal. As illustrated by this case report, a differential diagnosis of a metastatic malignant melanoma must be considered. 

Retracted: No

PubPeer comments:
 no double magnification ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,