PReD-Bench/PRed-Bench huggingface dataset:
Noncoding RNA miR‐205‐5p mediates osteoporosis pathogenesis and osteoblast differentiation by regulating RUNX2
Authors: Xiaowen Li
Can Zhou
Hongcheng Ding
Lianhua Chen
Mingwei Huang
Haiyan Zheng
Min Si
Journal: Journal of Cellular Biochemistry (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RUNX2; miR-205-5p; osteoblast differentiation; osteoporosis.
Affiliations: Department of Endocrinology, ShiYan People's Hospital & Affiliated People's Hospital of Hubei University of Medicine, Shiyan, Hubei, China., Department of Pharmacy, Affiliated People's Hospital of Hubei University of Medicine, China.

Abstract:  As a kind of noncoding RNAs, microRNAs (miRNAs) play important roles in disease pathogenesis by regulating gene expression. However, the molecular mechanism of miRNAs in osteoporosis remains largely unknown. In the present study, we aim to explore the genome-wide miRNAs expression profile and the regulatory mechanism of miR-205-5p in osteoporosis. A total of 72 differentially expressed miRNAs were identified in osteoporosis via microarray technology and bioinformatics analysis. We focused on one of the abnormally expressed miRNAs, miR-205-5p, which was previously unknown in osteoporosis. Quantitative real-time polymerase chain reaction (qRT-PCR) results showed that miR-205-5p was upregulated in osteoporosis samples and its expression was gradually decreased during osteogenic differentiation. Besides, miR-205-5p overexpression could inhibit the activity of osteoblast markers, including collagen, type I, α 1 (COL1A1) and alkaline phosphatase (ALP) while miR-205-5p inhibition showed the opposite results. Moreover, bioinformatics analysis identified the potential targets of miR-205-5p, including runt-related transcription factor 2 (RUNX2), SMAD1 and BCL6, etc. The dual-luciferase reporter assay confirmed RUNX2 was directly targeted by miR-205-5p. Furthermore, the rescue experiments showed that RUNX2 overexpression could significantly weaken the effect of miR-205-5p on osteoblast markers, indicating that miR-205-5p may inhibit osteogenic differentiation by targeting RUNX2. 

Retracted: No

PubPeer comments:
 In this article, electron microscopy (TEM) has been used to study insulin assemblies. It is known that low pH and high temperature is needed for insulin to form amyloid fibrils. Furthermore, dilution and sonication is needed in order to be able to study the samples by TEM. Without this treatment, you will get deposits that are too thick to be investigated by TEM (please see e.g. Krebs MRH et al., 2004, PNAS). In this article they used only high temperature and no dilution sonication is described for the TEM samples. I am wondering how the authors were able to perform TEM. The TEM images in Figure 6B are reused in Figure 9C, but flipped vertically. The treatment was different (72 h vs 48 h). ![file] , 
 #1 This has been addressed in the Corrigendum to u201cCapreomycin inhibits the initiation of amyloid fibrillation and suppresses amyloid induced cell toxicityu201d [Biochim. Biophy. Acta 1866 (2018) 549u2013557] . ,
The protective effects of dezocine on interleukin-1β-induced inflammation, oxidative stress and apoptosis of human nucleus pulposus cells and the possible mechanisms
Authors: Bing Ji
Chao Zhong
Wei Duan
Xinjun Liu
Fang Zhu
Journal: Bioengineered (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Intervertebral disc degeneration; dezocine; endoplasmic reticulum stress; human nucleus pulposus cells; inflammation
Affiliations: Department of Pain, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China, Dental Department, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China, Department of Vascular and Endovascular Surgery, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China

Abstract:  Intervertebral disc degeneration (IDD) is a natural problem linked to the inflammation. We aimed to investigate the role of dezocine (DEZ) in the development of IDD. Human nucleus pulposus cells (HNPCs) induced by interleukin (IL)-1β was used as a cellular model of IDD. After treatment with DEZ, HNPCs viability was evaluated with a CCK-8 assay. Then, the levels of inflammatory factors, including IL-6 and tumor necrosis factor-α (TNF-α), and oxidative stress-related markers, including reactive oxygen species (ROS), malondialdehyde (MDA) and reduced glutathione (GSH), were tested by RT-qPCR or kits. TUNEL staining was employed to detect cell apoptosis and Western blot was used to determine the expression of proteins related to inflammation, oxidative stress, apoptosis, endoplasmic reticulum stress (ERS) and MAPK signaling. Afterward, PMA, a MAPK signaling pathway agonist, was adopted for exploring the regulatory effects of DEZ on MAPK pathway. Results indicated that DEZ enhanced cell viability of HNPCs after IL-1β exposure. DEZ alleviated the inflammation and oxidative stress, evidenced by decreased levels of IL-6, TNF-α, ROS, MDA, p-NF-κB p65, NF-κB p65 in nucleus, cox-2 and increased levels of NF-κB p65 in cytoplasm, GSH, SOD1 and SOD2. Moreover, DEZ notably inhibited IL-1β-induced apoptosis of HNPCs. Furthermore, DEZ suppressed the levels of ERS-related proteins. The levels of related proteins in MAPK signaling including p-P38 and p-ERK1/2 were remarkably reduced after DEZ administration. By contrast, PMA crippled the impacts of DEZ on inflammation, oxidative stress and apoptosis of HNPCs induced by IL-1β. Collectively, DEZ ameliorates IL-1β-induced HNPCs injury via inhibiting MAPK signaling. 

Retracted: No

PubPeer comments:
 The lack of information regarding which qRT-PCR primers and antibodies and instruments used in this study, make it impossible to judge. The trustworthiness is low. There is no funding associated with this study, which is common for the many papermill papers from China. ![file] ,
Novel roles of unphosphorylated STAT3 in oncogenesis and transcriptional regulation
Authors: George R Stark
Karni Schlessinger
Hannah Nguyen
Jinbo Yang
Susan M Staugaitis
Moitreyee Chatterjee-Kishore
David E Levy
Journal: Cancer research (2005)
Discipline: CLINICAL MEDICINE
Keywords: STAT3; phosphorylation; gene expression; oncogene; unphosphorylated
Affiliations: Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio, USA.

Abstract:  Signal transducer and activator of transcription 3 (STAT3) is phosphorylated on tyrosine residue 705 in response to growth factors or cytokines to form activated homodimers that drive gene expression. Because the stat3 promoter has a binding site for STAT3 dimers, the amount of STAT3 protein increases when STAT3 is activated (e.g., in response to interleukin 6). Unphosphorylated STAT1 is known to drive the expression of certain genes. To explore the possibility of a similar role for the induced expression of unphosphorylated STAT3, we overexpressed either Y705F STAT3, which can not be phosphorylated on residue 705, or wild-type STAT3 in normal human mammary epithelial cells or STAT3-null mouse cells. The levels of many mRNAs were affected strongly by high levels of either form of STAT3. Some genes whose expression was increased by overexpressed STAT3, but not by activated STAT3 dimers, encode well-known oncoproteins (e.g., MRAS and MET). In many tumors, STAT3 is activated constitutively, and thus the unphosphorylated form is likely to be expressed highly, driving oncogene expression by a novel mechanism. In addition, expression of the stat3 gene is increased strongly in response to interleukin 6, and the high levels of unphosphorylated STAT3 that result drive a substantial late phase of gene expression in response to this cytokine. Thus, unphosphorylated STAT3, which activates gene expression by a novel mechanism distinct from that used by STAT3 dimers, is very likely to be an important transcription factor both in cancer and in responses to cytokines. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than you would expect, although the stated cell types are different. u00a0https: imgur.com aC1lrxa ,
Retracted : Long noncoding RNA TALNEC2 plays an oncogenic role in breast cancer by binding to EZH2 to target p57 KIP2 and involving in p‐p38 MAPK and NF‐κB pathways
Authors: Enqi Qiao
Weiliang Feng
Xiping Zhang
Qinglin Li
Daobao Chen
Ju Jin
Liang Xia
Xingfei Yu
Hongjian Yang
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: EZH2; TALNEC2; breast cancer; p-p38 MAPK and NF-κB pathways; p57KIP2.
Affiliations: Department of Breast Surgery, Zhejiang Cancer Hospital, Hangzhou, China., Department of Pharmacy, Zhejiang Cancer Hospital, Hangzhou, China., Department of Cerebral Surgery, Zhejiang Cancer Hospital, Hangzhou, China.

Abstract:  We aimed to investigate the potential role and regulatory mechanism of long noncoding RNA tumor-associated lncRNA expressed in chromosome 2 (TALNEC2) in breast cancer. The expression of TALNEC2 in breast cancer tissues and cells were investigated. MCF-7 and MDA-MB-231 cells were transfected with small interfering RNA (siRNA) duplexes for targeting TALNEC2 (si-TALNEC2), enhancer of zeste homolog 2 (EZH2; si-EZH2) and p57KIP2 (si-p57 KIP2 ), and their corresponding controls (si-NC). The viability, colony forming ability, cell cycle, apoptosis, and autophagy of transfected cells were assessed. The expressions of p-p38 mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathway-related proteins were investigated. The results showed that TALNEC2 was highly expressed in breast cancer tissues and cells. Knockdown of TALNEC2 significantly inhibited the malignant behaviors of MCF-7 and MDA-MB-231 cells, including inhibiting cell viability and colony forming, arresting cell cycle at G0/G1 phase, inducing cell apoptosis, and promoting cell autophagy. EZH2 was a TALNEC2 binding protein, which was upregulated in breast cancer tissues and cells and could negatively regulate p57 KIP2 . Effects of TALNEC2 knockdown on malignant behaviors of MCF-7 cells were reversed by p57 KIP2 knockdown. The expressions of p-p38, RelA, and RelB in MCF-7 cells were decreased after knockdown of TALNEC2 or EZH2, which were reversed by knockdown of p57 KIP2 concurrently. In conclusion, TALNEC2 may play an oncogenic role in breast cancer by binding to EZH2 to target p57 KIP2 . Activation of p-p38 MAPK and NF-κB pathways may be key mechanisms mediating the oncogenic role of TALNEC2 in breast cancer. TALNEC2 may serve as a promising target in the therapy of breast cancer. 

Retracted: Yes

PubPeer comments:
 The mouse image in Figure 5f has been slightly cropped and reused in Figure 6c. ![file] , 
 #1 Thanks for the comment. As mentioned in the paper, the mouse in Figure 5f and 6c is a same one. ,
Metal-free green synthesis of aryl amines in magnetized distilled water: experimental aspects and molecular dynamics simulation
Authors: Mohammad Bakherad
Zainab Moosavi-Tekyeh
Amin Rezaeifard
Rahele Doosti
Nasrin Mehmandoost
Naser Goudarzi
Sima Omara
Journal: Green Chemistry (2020)
Discipline: CHEMISTRY
Keywords: N-arylation; secondary amines; aryl halides; magnetized distilled water; solvent
Affiliations: Faculty of Chemistry, Shahrood University of Technology, Shahrood 3619995161, Iran

Abstract: In this work, a simple, green, and transition metal-free approach to the N-arylation of secondary amines with aryl halides in magnetized distilled water (MDW), as a solvent, is introduced. This method offers the advantages of short reaction times, low costs, and an additive-free process, and it also enables new planning strategies for the construction of aryl amine-containing pharmacophores. Also, the reaction rates were followed spectrophotometrically by monitoring the changes in the absorption spectrum of the reaction mixture in ordinary and magnetized distilled water. Furthermore, we used the reliable molecular dynamics (MD) simulations as predictive tools to interpret and describe the interactions between reactants in the ordinary and magnetized distilled water. The RDFs analysis of interactions revealed that morpholine and iodobenzene reactants were surrounded by more solvents in MDW than ordinary distilled water (ODW) 90 °C. Consequently, the high reactivity observed for two reactants in MDW at 90 °C can be explained by MD simulation, and there comes an established synergy between the theoretical calculation and experiment.

Retracted: Yes

PubPeer comments:
 Figure 2A. When the 96h High Mag image is scaled down 5:1 sarcomeric striations are still clearly visible, yet no sarcomeric striations are apparent in the 96 h (standard magnification for all other images in figure 2A) image. ![file] ,
Gastroprotective Properties of Karanjin from Karanja (Pongamia pinnata) Seeds; Role as Antioxidant and H+, K+-ATPase Inhibitor
Authors: Vinay B Jayaram
Sindhu Rajashekhar
Srikanta M Belagihally
Shylaja M Dharmesh
Vismaya
Sindhu Kanya C Thirumakudalu
Journal: Evidence-based Complementary and Alternative Medicine (2011)
Discipline: CLINICAL MEDICINE
Keywords: Plant extracts; newer drugs; gastric ulcers; Karanjin; anti-ulcerogenic property
Affiliations: Department of Protein Chemistry and Technology, Central Food Technological Research Institute, CSIR, Mysore 570020, Karnataka, India., Department of Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR, Mysore 570020, Karnataka, India, Department of Protein Chemistry and Technology, Central Food Technological Research Institute, CSIR, Mysore 570020, Karnataka, India

Abstract:  Plant extracts are the most attractive sources of newer drugs and have been shown to produce promising results for the treatment of gastric ulcers. Karanjin, a furano-flavonoid has been evaluated for anti-ulcerogenic property by employing adult male albino rats. Karanjin (&gt;95% pure) was administered to these rats in two different concentrations, that is, 10 and 20 mg kg(-1) b.w. Ulcers were induced in the experimental animals by swim and ethanol stress. Serum, stomach and liver-tissue homogenates were assessed for biochemical parameters. Karanjin inhibited 50 and 74% of ulcers induced by swim stress at 10 and 20 mg kg(-1) b.w., respectively. Gastric mucin was protected up to 85% in case of swim stress, whereas only 47% mucin recovery was seen in ethanol stress induced ulcers. H(+), K(+)-ATPase activity, which was increased 2-fold in ulcer conditions, was normalized by Karanjin in both swim/ethanol stress-induced ulcer models. Karanjin could inhibit oxidative stress as evidenced by the normalization of lipid peroxidation and antioxidant enzyme (i.e., catalase, peroxidase and superoxide dismutase) levels. Karanjin at concentrations of 20 mg kg(-1) b.w., when administered orally for 14 days, did not indicate any lethal effects. There were no significant differences in total protein, serum glutamate pyruvate transaminase, serum glutamate oxaloacetate transaminase and alkaline phosphatase between normal and Karanjin-treated rats indicating no adverse effect on major organs. During treatment schedule, animals remained as healthy as control animals with normal food and water intake and body weight gain. 

Retracted: No

PubPeer comments:
 unexpected image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Construction and evaluation of a prognosis lncRNA model for hepatocellular carcinoma
Authors: Yanling Chen
Xiaofei Xue
Shasha Li
Zujiang Yu
Fulei Li
Lu Bai
Journal: Journal of Cellular Biochemistry (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: GSEA; ROC; hepatocellular carcinoma; lncRNA; nomogram
Affiliations: Department of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China., Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Abstract:  Current studies indicate that long non-coding RNA (lncRNA) is often abnormally expressed in hepatocellular carcinoma (HCC). We intend to generate a multi-lncRNA signal to improve the prognosis of HCC. By analyzing 12 pairs of HCC and adjacent normal mucosal tissues, 3900 differentially expressed lncrnas were identified as candidate biomarkers for the prognosis of HCC. Then, the 12-lncrna signature was constructed using the LASSO Cox regression method and verified in the TCGA training dataset. Finally, we established a novel 12-lncrna signature that was significantly associated with overall survival (OS) in the training data set. With the use of 12-lncrna markers, patients in the training cohort were divided into high-risk and low-risk groups with significant OV differences (P &lt; .0001). Similar results were consistent in the TCGA verification dataset (P = .046). Multivariate Cox model was used to analyze and construct the risk scores of selected key lncRNA and AJCC stages. The results showed that, compared with AJCC stages, lncRNA-based risk scores were another important factor affecting the OS of patients. We found that risk scores based on lncRNA have a stronger prediction ability than the AJCC stage alone on 4-year OS. For 4-year survival rates, prediction combined with the lncRNA risk score and AJCC stage, model effectiveness (sensitivity and specificity) has reached to 0.750. To further explore the biological processes involved in prognostic lncRNA, all HCC samples in TCGA are divided into two groups according to the median lncRNA risk score, and analyzed the gene enrichment of high expression genes and low expression genes in KEGG data using goana in limma. The results suggest that the genes associated with tumor pathways, such as PI3K-Akt and ECM-receptor interaction, are highly expressed in the high risk group. 

Retracted: No

PubPeer comments:
 Figure 5B More similar than expected, could authors check it please? ![file] ,
Glycolysis in Panc-1 human pancreatic cancer cells is inhibited by everolimus
Authors: Liansheng Gong
Nianfeng Li
Yangde Zhang
Ling Liu
Journal: Experimental and Therapeutic Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: everolimus; Panc-1; pancreatic cancer cells; apoptosis; glycolysis
Affiliations: National Hepatobiliary and Enteric Surgery Research Center, Xiangya Hospital, Central South University, Changsha, Hunan 410008,  P.R. China.

Abstract:  The aim of this study was to evaluate the effects and molecular mechanisms of everolimus on Panc-1 human pancreatic cancer cells. Panc-1 human pancreatic cancer cells were treated with everolimus (10 μg/ml) at selected time points (6, 12 and 24 h). Cell proliferation and apoptosis were evaluated by MTT and flow cytometric analyses. The glycolytic activity was determined by measuring the activity of the key enzyme lactate dehydrogenase (LDH) and lactate production. The activity of mammalian target of rapamycin (mTOR) signaling was measured by western blotting. The expression of genes, including hexokinase 2 (HK2) and microRNA-143 (miR-143), was evaluated by real-time polymerase chain reaction (PCR). The administration of everolimus time-dependently inhibited proliferation and glycolysis and induced apoptosis in the Panc-1 human pancreatic cancer cells. As the time of treatment with everolimus increased, the mTOR signaling activity decreased, indicated by lower phosphorylation levels of S6 kinase; however, the phosphorylation levels of mTOR barely changed. Moreover, our data showed an everolimus-induced increase in miR-143 and decrease in HK2 in Panc-1 cells in a time-dependent manner. In conclusion, the current study indicates a novel role of everolimus in its antitumor effect as an inhibitor of glycolysis in Panc-1 human pancreatic cancer cells. Furthermore, our data highlights the significance of exploring the mechanisms of everolimus and miR-143 in malignant tumors. 

Retracted: No

PubPeer comments:
 Figure 2.  Everolimus induced cell apoptosis in Panc-1 pancreatic cancer cells. Following treatment of Panc-1 cells with 10 u00b5g ml everolimus for 6, 12 and 24 h, apoptotic cells were detected by Annexin V and PI double staining. ![file] Other manifestations of these panels include Figs 2C; 4B of [He et al (2015)] . ![file] Figs 1C, 4D from [Zhao et al (2015)] .  Overexpression of miR-148a promoted paclitaxel-induced cell apoptosis, whereas inhibition of miR-148a suppressed paclitaxel-induced cell apoptosis, compared with the control group ;  Overexpression of PDIA3 inhibited paclitaxel-induced cell apoptosis, whereas inhibition of PDIA3 promoted paclitaxel-induced cell apoptosis, compared with the control . ![file] ,
Curcumin improves the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cells via the NF-κB-p53-caspase-3 pathway
Authors: Rong Tian
Xiao-Ying Yuan
Dong-Guang Li
Wei Liu
Yu-Ping Dang
Journal: Experimental and Therapeutic Medicine (2015)
Discipline: CLINICAL MEDICINE
Keywords: NF-κB-p53-caspase-3 pathway; apoptosis; cervical cancer cells; curcumin.
Affiliations: Department of Dermatology, Air Force General Hospital of People's Liberation Army, Beijing 100142, P.R. China.

Abstract:  Paclitaxel, isolated from Taxus brevifolia, is considered to be an efficacious agent against a wide spectrum of human cancers, including human cervical cancer. However, dose-limiting toxicity and high cost limit its clinical application. Curcumin, a nontoxic food additive, has been reported to improve paclitaxel chemotherapy in mouse models of cervical cancer. However, the underlying mechanisms remain unclear. In this study, two human cervical cancer cell lines, CaSki [human papilloma virus (HPV)16-positive] and HeLa (HPV18-positive), were selected in which to investigate the effect of curcumin on the anticancer action of paclitaxel and further clarify the mechanisms. Flow cytometry and MTT analysis demonstrated that curcumin significantly promoted paclitaxel-induced apoptosis and cytotoxicity in the two cervical cell lines compared with that observed with paclitaxel alone (P&lt;0.05). Reverse transcription-polymerase chain reaction indicated that the decline of HPV E6 and E7 gene expression induced by paclitaxel was also assisted by curcumin. The expression levels of p53 protein and cleaved caspase-3 were increased significantly in the curcumin plus paclitaxel-treated HeLa and CaSki cells compared with those in the cells treated with paclitaxel alone (P&lt;0.01). Significant reductions in the levels of phosphorylation of IκBα and the p65-NF-κB subunit in CaSki cells treated with curcumin and paclitaxel were observed compared with those in cells treated with paclitaxel alone (P&lt;0.05). This suggests that the combined effect of curcumin and paclitaxel was associated with the NF-κB-p53-caspase-3 pathway. In conclusion, curcumin has the ability to improve the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cell lines via the NF-κB-p53-caspase-3 pathway. Curcumin in combination with paclitaxel may provide a superior therapeutic effect on human cervical cancer. 

Retracted: No

PubPeer comments:
 Figure 1. Some groups of dots appear to be visible multiple times within or across panels. Boxes of the same color highlight some of these areas. ![file] ,
Olanzapine inhibits the proliferation and induces the differentiation of glioma stem-like cells through modulating the Wnt signaling pathway in vitro
Authors: H-J Yang
Q-H Guo
S-D Wang
Journal: European review for medical and pharmacological sciences (2015)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Olanzapine; proliferation; differentiation; glioma stem-like cells; Wnt signaling pathway
Affiliations: Department of Pediatrics, The Second Hospital of Shandong University, Jinan, Shandong, China. .

Abstract:  The article "Olanzapine inhibits the proliferation and induces the differentiation of glioma stem-like cells through modulating the Wnt signaling pathway in vitro" by Q.-H. Guo, H.-J. Yang, S.-D. Wang, published in Eur Rev Med Pharmacol Sci 2013; 19 (13): 2406-2415 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
TGFbeta3 inhibits E-cadherin gene expression in palate medial-edge epithelial cells through a Smad2-Smad4-LEF1 transcription complex
Authors: Elizabeth D Hay
Chang-Chih Liu
Ali Nawshad
Damian Medici
Journal: Journal of Cell Science (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MEE; palate development; TGFbeta3; E-cadherin; LEF1
Affiliations: Department of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NE 68583, USA. , Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA, Department of Oral Biology, College of Dentistry, University of Nebraska Medical Center, Lincoln, NE 68583, USA

Abstract:  Dissociation of medial-edge epithelium (MEE) during palate development is essential for mediating correct craniofacial morphogenesis. This phenomenon is initiated by TGFbeta3 upon adherence of opposing palatal shelves, because loss of E-cadherin causes the MEE seam to break into small epithelial islands. To investigate the molecular mechanisms that cause this E-cadherin loss, we isolated and cultured murine embryonic primary MEE cells from adhered or non-adhered palates. Here, we provide the first evidence that lymphoid enhancer factor 1 (LEF1), when functionally activated by phosphorylated Smad2 (Smad2-P) and Smad4 (rather than beta-catenin), binds with the promoter of the E-cadherin gene to repress its transcription in response to TGFbeta3 signaling. Furthermore, we found that TGFbeta3 signaling stimulates epithelial-mesenchymal transformation (EMT) and cell migration in these cells. LEF1 and Smad4 were found to be necessary for up-regulation of the mesenchymal markers vimentin and fibronectin, independently of beta-catenin. We proved that TGFbeta3 signaling induces EMT in MEE cells by forming activated transcription complexes of Smad2-P, Smad4 and LEF1 that directly inhibit E-cadherin gene expression. 

Retracted: No

PubPeer comments:
 The bands of different groups in red boxes in Fig 4 appear to look similar. ![file] , 
 We are so sorry for not taking notice of this message, in time. Thank you for your comment. In this paper, the right panel of Figure 4H presents a negative experiment which shows His-Mju03b2arr-N does not interact with GST-MjCactus-N-ANK. As you have pointed, this figure seems similar with the right panel of Figure 4I. We have revisted the raw data of these experiments. The corrected Figure4H right panel and related raw data are attached below. We sincerely apologize for this unintentional error made before manuscript submission but we failed to catch at the submission and subsequent review and publication steps. ![file] ![file] , 
 To show the results more clearly, we provide the corrected Figure 4H and the raw data of Figure4H right panel. ![file] ,
Sappanone A prevents hypoxia-induced injury in PC-12 cells by down-regulation of miR-15a
Authors: Xiaoyang Liu
Yao Fu
Mingyang Kang
Libo Wang
Chunyang Kang
Jian Gao
Journal: International Journal of Biological Macromolecules (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cerebral ischemia; Hypoxia; Sappanone A.
Affiliations: Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130000, China., Department of Neurosurgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130000, China., Department of Spine Surgery, The Second Hospital of Jilin University, Changchun, Jilin, 130000, China., Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, 130000, China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editors-in-Chief. Given the comments regarding this article “The only experimental results presented in this paper are stylised, conventionalised 'western blots' that in fact resemble playful sardines, or tadpoles’, the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editors-in-Chief decided to retract the article. 

Retracted: Yes

PubPeer comments:
 The only experimental results presented in this paper are stylised, conventionalised western blots that in fact resemble playful sardines, or tadpoles. ![file] , 
 Retracted [11 February 2022] . ----------------------------- This article has been retracted at the request of the Editors-in-Chief. Given the comments regarding this article u201cThe only experimental results presented in this paper are stylised, conventionalised western blots that in fact resemble playful sardines, or tadpolesu2019, the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editors-in-Chief decided to retract the article. ,
Withaferin a strongly elicits IkappaB kinase beta hyperphosphorylation concomitant with potent inhibition of its kinase activity
Authors: Mary Kaileh
Jacques Piette
Tamer Essawi
Julie Horion
Wim Vanden Berghe
Arne Heyerick
Guy Haegeman
Denis De Keukeleire
Claude Libert
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: NFkappaB; drug development; Withania somnifera; inflammatory disorders; withaferin A
Affiliations: Laboratory of Eukaryotic Gene Expression and Signal Transduction (LEGEST), Department of Molecular Biology, Ghent University-UGent, K. L. Ledeganckstraat 35, B-9000 Gent, Belgium.

Abstract:  The transcription factor NFkappaB plays a critical role in normal and pathophysiological immune responses. Therefore, NFkappaB and the signaling pathways that regulate its activation have become a major focus of drug development programs. Withania somnifera (WS) is a medicinal plant that is widely used in Palestine for the treatment of various inflammatory disorders. In this study we show that the leave extract of WS, as well as its major constituent withaferin A (WA), potently inhibits NFkappaB activation by preventing the tumor necrosis factor-induced activation of IkappaB kinase beta via a thioalkylation-sensitive redox mechanism, whereas other WS-derived steroidal lactones, such as withanolide A and 12-deoxywithastramonolide, are far less effective. To our knowledge, this is the first communication of IkappaB kinase beta inhibition by a plant-derived inhibitor, coinciding with MEK1/ERK-dependent Ser-181 hyperphosphorylation. This prevents IkappaB phosphorylation and degradation, which subsequently blocks NFkappaB translocation, NFkappaB/DNA binding, and gene transcription. Taken together, our results indicate that pure WA or WA-enriched WS extracts can be considered as a novel class of NFkappaB inhibitors, which hold promise as novel anti-inflammatory agents for treatment of various inflammatory disorders and/or cancer. 

Retracted: No

PubPeer comments:
 Figure 1. Much more similar than you would expect. Slight difference in exposure. https: imgur.com NbnyofY ,
lncRNA-RMRP promotes proliferation, migration and invasion of bladder cancer via miR-206
Authors: Z-J Liu
J-N Xi
P-L Huang
Y-L Yue
H-L Cao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Bladder cancer; lncRNA-RMRP; proliferation; migration; invasion
Affiliations: Beijing Rehabilitation Hospital Affiliated to Capital Medical University, Beijing, China. .

Abstract:  Objective: The incidence of bladder cancer (BC) is common in the world, but its detail mechanisms for occurrence and development remain unclear. Recently, long non-coding RNAs (lncRNAs) have been observed to play an important role in many different diseases. In this research, we mainly explored the role of the RNA component of mitochondrial RNA processing endoribonuclease (lncRNA-RMRP) in bladder cancer. Materials and methods: We used qRT-PCR to detect the expression of lncRNA-RMRP in bladder cancer patients and tumor cells, and the clinical significance was also analyzed. The methyl thiazolyl tetrazolium (MTT) assay was used to detect the cell proliferation, and we used transwell to detect the migration and invasion, after the lncRNA RMRP was inhibited. Western-blot was used to measure the relative protein expression level in bladder cancer cells after transfection with siRNA-NC or siRNA-RMRP. Results: We found that the lncRNA RMRP was highly expressed in bladder cancer tissue, compared with adjacent tissue. We also found that the expression of RMRP was closely related with the size, lymph node metastasis and survival time of patients. What's more, RMRP could promote the proliferation, migration and invasion of BC cell lines via regulating miR-206 as a sponge. Conclusions: According to the results, we found that lncRNA RMRP was closely related to the progression of bladder cancer, which could be a potential target for treating BC patients. 

Retracted: No

PubPeer comments:
 From the Methods:  91 cases of bladder cancer (BC) tissue and adjacent tissue were collected from Beijing Rehabilitation Hospital Affiliated to Capital Medical University in Beijing City (Beijing, China) from May 2016 to June 2017.  The paper was published in February 2019, three years after recruitment of the first patients. Yet, Figure 2C shows that the patients were followed for more than 5 years ( 60 months). Could the authors please clarify how this is possible? ![file] , 
 One year passed, still not response from the authors. Let me add some more: From the start of the Introduction:  Bladder cancer (BC) is the most common malignant tumor in the urinary system and it is the fourth of male malignant tumors in European and American countries1. Ref 1: Bizhani F et al. Association between single nucleotide polymorphisms in the PI3K Akt mTOR pathway and bladder cancer risk in a sample of Iranian population. EXCLI J 2018: 3-13. ,
Homeodomain-containing gene 10 contributed to breast cancer malignant behaviors by activating Interleukin-6/Janus kinase 2/Signal transducer and activator of transcription 3 pathway
Authors: Jun Zhou
Jun Shen
Huanhuan Yan
Meng Wang
Fan Li
Journal: Bioengineered (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: HOXC10; IL-6; JAK2/STAT3 pathway; breast cancer.
Affiliations: Department of Breast Surgery, The First People’s Hospital of LianYunGang, Lianyungang, Jiangsu Province, China

Abstract:  Homeodomain‑containing gene 10 (HOXC10) has been identified as an oncogene in various malignancies. Nevertheless, the role and function of HOXC10 in breast cancer (BC) remain unclear. RT-qPCR and Western blot were used to detect the mRNA and protein levels of genes, respectively. CCK-8, transwell, and TUNEL assays were performed to evaluate cell viability, invasion, migration, and apoptosis of BC cells in vitro. The xenograft model was established to examine the effect of HOXC10 on tumor growth in vivo. Our results indicated that HOXC10 expression was increased in BC and correlated with an unsatisfactory prognosis. Functional assays indicated that HOXC10 overexpression promoted cell proliferation and metastasis, and suppressed cell apoptosis of BC, while HOXC10 knockdown showed opposite trends. Furthermore, in vitro and in vivo assays uncovered that HOXC10 promoted the tumorigenesis of BC via the activation of IL-6/JAK2/STAT3 signaling. Overall, our study revealed that HOXC10 could function as a tumor promotor in BC by upregulating IL-6 levels to activate the JAK2/STAT3 signaling pathway. 

Retracted: No

PubPeer comments:
 Details regarding the patients involved in this study are lacking (type of breast cancer tissue collected, when tissue was collected and approval number), as well as essential details regarding much of the methods (qRT-PCR primer seqences, secondary antibody and instrument used to read the ECL signal in Western blotting etc). Can the authors please provide this information? Furthermore, the cell viability data look pretty extraordinary. Are the cells actually waking up from the death? Common for many Bioenginereed papers, other Bioenginereed papers are quoted for no reason. It s hardly coincidental that these are often in order, and from the same journal issue (2021; 12). There is an error in the presentation of several of the micrographs in Figure 2f. Last reason to be concerned regarding this paper is the fact that there is no funding associated with this rather comprehensive study. This is highly unusual, but in the many falsified papermill paper we previously identified from China, this is common. ![file] ,
miR-130 aggravates acute myocardial infarction-induced myocardial injury by targeting PPAR-γ
Authors: Xiaotian Sun
Xiaofeng Chen
Jiechun Huang
Xianglin Chu
Yiqing Wang
Liewen Pang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PPAR-γ; acute myocardial infarction; inflammation; miR-130; myocardial fibrosis.
Affiliations: Department of Cardiothoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.

Abstract:  Cardiac remodeling is a common pathophysiological change associated with acute myocardial infarction (AMI). Recent evidence indicates that microRNAs are strong posttranscriptional regulators which play an important role in regulating the microenvironment of myocardial tissue after AMI. In this study, we sought to explore the potential role and underlying mechanism of miR-130 in AMI. H9c2 cells were cultured under hypoxic conditions to simulate myocardial infarction. The influence of aberrantly expressed miR-130 on H9c2 cells under hypoxia was also estimated with RT-PCR, western blot and enzyme-linked immunosorbent assay. Using bioinformatics methods, of miR-130 target genes were verified with luciferase reporter assay. Then, the effects of miR-130 on AMI were identified in an induced myocardial injury model in rats. The results show that miR-130 downregulation remarkably decreased hypoxia-induced inflammation and fibrosis related protein expression in H9c2 cells and reversed hypoxia-induced peroxisome proliferator-activated receptor γ (PPAR-γ) inhibition. A bifluorescein reporter assay further confirmed that PPAR-γ was a target gene of miR-130. This study verified that PPAR-γ has a cardioprotective effect by inhibiting NFκB-mediated inflammation and TGF-β1-mediated fibrosis. In vivo experiments confirmed that downregulation of miR-130 expression promotes PPAR-γ-mediated cardioprotective effects by suppressing inflammation and myocardial fibrosis. Taken together, these findings suggest that miR-130 knockdown alleviates infarction-induced myocardial injury by promoting PPAR-γ expression. 

Retracted: No

PubPeer comments:
 Figures 1B, 2G. The marked panels have more points in common around their fringes than one would expect. ![file] Here dramatised by colour-inverting the  Hypoxia panel and superimposing it upon  hypoxia + inhibitor . A few areas of coincidence cancellation are marked. ![file] ,
Cytotoxic and Inflammatory Responses Induced by Outer Membrane Vesicle-Associated Biologically Active Proteases from Vibrio cholerae
Authors: Ayan Mondal
Amit Ghosh
Amit Pal
Hemanta Koley
Nabendu Sekhar Chatterjee
Rima Tapader
Ritam Sinha
Sun Nyunt Wai
Manoj K Chakrabarti
Dhira Rani Saha
Journal: Infection and Immunity (2016)
Discipline: IMMUNOLOGY
Keywords: Proteases; Vibrio cholerae; pathogenesis; Zn-dependent hemagglutinin protease; calcium-dependent trypsin-like serine protease
Affiliations: Division of Pathophysiology, National Institute of Cholera and Enteric Diseases, Kolkata, India., Division of Biochemistry, National Institute of Cholera and Enteric Diseases, Kolkata, India., Division of Bacteriology, National Institute of Cholera and Enteric Diseases, Kolkata, India., Histology and Electron Microscopy, National Institute of Cholera and Enteric Diseases, Kolkata, India., Department of Molecular Biology, Umea Centre of Microbial Research, Umea University, Umea, Sweden., Division of Pathophysiology, National Institute of Cholera and Enteric Diseases, Kolkata, India .

Abstract:  Proteases in Vibrio cholerae have been shown to play a role in its pathogenesis. V. cholerae secretes Zn-dependent hemagglutinin protease (HAP) and calcium-dependent trypsin-like serine protease (VesC) by using the type II secretion system (TIISS). Our present studies demonstrated that these proteases are also secreted in association with outer membrane vesicles (OMVs) and transported to human intestinal epithelial cells in an active form. OMV-associated HAP induces dose-dependent apoptosis in Int407 cells and an enterotoxic response in the mouse ileal loop (MIL) assay, whereas OMV-associated VesC showed a hemorrhagic fluid response in the MIL assay, necrosis in Int407 cells, and an increased interleukin-8 (IL-8) response in T84 cells, which were significantly reduced in OMVs from VesC mutant strain. Our results also showed that serine protease VesC plays a role in intestinal colonization of V. cholerae strains in adult mice. In conclusion, our study shows that V. cholerae OMVs secrete biologically active proteases which may play a role in cytotoxic and inflammatory responses. 

Retracted: No

PubPeer comments:
 It is clearly visible that spliced lanes were joined to create the panel. Backgrounds of the two spliced lanes were significantly different. ![file] ,
Magnesium–zinc–calcium–vitamin D co-supplementation improves glycemic control and markers of cardiometabolic risk in gestational diabetes: a randomized, double-blind, placebo-controlled trial
Authors: Shahla Bahramimoghadam
Maryam Karamali
Zatollah Asemi
Fateme Sharifzadeh
Journal: Applied Physiology Nutrition and Metabolism (2018)
Discipline: CLINICAL MEDICINE
Keywords: cardiometabolic risk; contrôle glycémique; diabète gestationnel; gestational diabetes mellitus; glycemic control
Affiliations: Department of Gynecology and Obstetrics, School of Medicine, Iran University of Medical Sciences, Tehran, Iran., Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran.

Abstract:  To the best our knowledge, data on the effects of magnesium-zinc-calcium-vitamin D co-supplementation on glycemic control and markers of cardiometabolic risk in gestational diabetes mellitus (GDM) are scarce. The purpose of this study was to establish the effects of magnesium-zinc-calcium-vitamin D co-supplementation on glycemic control and markers of cardiometabolic risk of GDM patients. Sixty patients with GDM, aged 18-40 years, were randomized into 2 groups to intake either magnesium-zinc-calcium-vitamin D co-supplements or placebo (n = 30 each group) for 6 weeks in a randomized, double-blind, placebo-controlled trial. Fasting blood samples were taken at baseline and week 6 to quantify related markers. After the 6-week intervention, compared with the placebo, magnesium-zinc-calcium-vitamin D co-supplementation resulted in significant reductions in fasting plasma glucose (-0.37 ± 0.09 vs. +0.01 ± 0.09 mmol/L, P = 0.003), serum insulin levels (-21.0 ± 4.8 vs. +7.2 ± 4.8 pmol/L, P &lt; 0.001), homeostatic model of assessment for insulin resistance (-1.0 ± 1.1 vs. +0.3 ± 1.3, P &lt; 0.001), and a significant increase in quantitative insulin sensitivity check index (+0.02 ± 0.03 vs. -0.002 ± 0.03, P = 0.003). In addition, magnesium-zinc-calcium-vitamin D co-supplementation significantly decreased serum triglycerides (-0.25 ± 0.10 vs. +0.34 ± 0.10 mmol/L, P = 0.001) and very-low-density-cholesterol concentrations (-0.11 ± 0.04 vs. +0.15 ± 0.04 mmol/L, P = 0.001) compared with the placebo. Overall, the results of this study demonstrated that magnesium-zinc-calcium-vitamin D co-supplementation for 6 weeks among patients with GDM had beneficial effects on glycemic control and few markers of cardiometabolic risk. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A142 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 18 publications have an expression of concern, and 6 have been retracted. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Effect of central administration of QRFP(26) peptide on energy balance and characterization of a second QRFP receptor in rat
Authors: J Kampe
P T Pfluger
M H Tschöp
P Wiedmer
H Mondala
L Burget
J Kerr
D Bagnol
B J Oldfield
T R Castaneda
C Liaw
Journal: Brain Research (2006)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: neuropeptide; QRFP(26); hypothalamus; food intake; GPR103
Affiliations: Department of Psychiatry, Obesity Research Center, University of Cincinnati-Genome Research Institute, Cincinnati, OH, USA.

Abstract:  The recently identified neuropeptide QRFP(26) is predominantly expressed in the hypothalamus and was suggested to play a role in the regulation of food intake following the observation of an acute orexigenic effect after central administration in mice. QRFP(26) exerts its effect via GPR103 and a newly identified receptor in mouse. The aim of our study was (a) to investigate the distribution of QRFP(26) and a newly discovered QRFP receptor mRNA in rat and (b) to further characterize the effects of central administration of QRFP(26) on energy balance in rats. QRFP(26) mRNA was detected in the retrochiasmatic nucleus, periventricular nucleus, arcuate nucleus and restricted areas of the lateral nucleus of the hypothalamus. We found an additional receptor with high homology for GPR103 in rat. This receptor increases inositol triphosphate production in transfected cells in presence of QRFP(26) and its mRNA was particularly enriched in ventral and posterior thalamic groups, anterior hypothalamus and medulla. When QRFP(26) (10 microg and 50 microg) was administered centrally before the start of the light phase both doses increased food intake for 2 h after injection without reaching statistical significance. QRFP(26) caused no changes in locomotor activity or energy expenditure. In summary, central QRFP(26) injection causes slight and transient hyperphagia in rats without changing any other energy balance parameters after 24 h. We conclude that QRFP(26) has limited impact on the central regulation of energy balance in rats and that its essential function remains to be clarified. 

Retracted: No

PubPeer comments:
 fig 4 L with some duplications after increasing brightness ![file] , 
 #1 ![file] , 
 This autoradiographic montage was obtained by exposing a rat brainstem section mounted on a microscopic slide with a QRFP-r2 or GPR103B mRNA antisense probe labeled with 33P-UTP. The slide was exposed to a radioactive sensitive film, developed, and digitalized to generate color-coded or black white autoradiograms. A rat brainstem section autoradiogram labeled with QRFP-r2 mRNA probe was cut out and paste on an autoradiographic film background for illustration. The labeling in the hypoglossal nucleus and inferior olive is specific and evident also in figure 4K. The use of sense probes for QRFP-r2 did not show any labeling in those nuclei or other brain areas. The original picture is attached below. ![file] , 
 There is some evidence that parts of #3 has been used to construct image #2 while it does not explain the duplications initially found by #1. Could we please see the full #3 image? ![file] ,