Molecular medicine reports最新文献

{"title":"Swimming training promotes angiogenesis of endothelial progenitor cells by upregulating IGF1 expression and activating the PI3K/AKT pathway in type 2 diabetic rats.","authors":"Lan Li, Xiao-Ying Mang, Ke-Wei Jiang, Ying Zhao, Yu-Rong Chen","doi":"10.3892/mmr.2024.13361","DOIUrl":"10.3892/mmr.2024.13361","url":null,"abstract":"<p><p>The present study aimed to investigate the effect of swimming training on the angiogenesis of endothelial progenitor cells (EPCs) in type 2 diabetes mellitus (T2DM) rats by upregulating the insulin‑like growth factor 1 (IGF1) expression and to reveal its potential mechanism of action. Male Sprague‑Dawley rats were divided into the Control, Model, Model train, Model train + short interfering (si)‑NC and Model train + si‑IGF1 groups. Serum glucose levels were measured using the oral glucose tolerance test. EPCs were isolated from the bone marrow cavity and identified through morphological observation and immunofluorescence staining. The expression of IGF‑1 mRNA in rat serum and EPCs was analyzed by reverse transcription‑quantitative PCR. The fasting insulin levels in serum were assessed by ELISA. Cell Counting Kit‑8, scratch assay and tube formation assay were used to determine the cell viability, migration and tube formation of rat EPCs, and western blotting was employed to measure the expression levels of IGF1, phosphoinositide 3‑kinase (PI3K), phosphorylated‑PI3K, protein kinase B (AKT) and phosphorylated‑AKT. The present study demonstrated that swimming training significantly decreased the glucose levels and homeostatic model assessment of insulin resistance scores, but increased the fasting insulin levels and IGF1 mRNA expression. Microscopic observation and immunofluorescence identification suggested that EPCs were successfully isolated. In addition, swimming training markedly elevated the levels of IGF1 and promoted cell viability, migration and tube formation in rat EPCs. Furthermore, IGF1 knockdown experiments indicated that swimming training might play a regulatory role by elevating the IGF1 expression to activate the PI3K/AKT pathway. Overall, swimming training promoted the angiogenesis of EPCs in T2DM rats and its potential mechanism may be related to the upregulation of IGF1 expression and the activation of the PI3K/AKT pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cisplatin‑resistant germ cell tumor models: An exploration of the epithelial‑mesenchymal transition regulator <i>SLUG</i>.","authors":"Ingridy Izabella Vieira Cardoso, Marcela Nunes Rosa, Daniel Antunes Moreno, Letícia Maria Barbosa Tufi, Lorrayne Pereira Ramos, Larissa Alessandra Bourdeth Pereira, Lenilson Silva, Janaina Mello Soares Galvão, Isabela Cristiane Tosi, André Van Helvoort Lengert, Marcelo Cavalcanti Da Cruz, Silvia Aparecida Teixeira, Rui Manuel Reis, Luiz Fernando Lopes, Mariana Tomazini Pinto","doi":"10.3892/mmr.2024.13352","DOIUrl":"10.3892/mmr.2024.13352","url":null,"abstract":"<p><p>Germ cell tumors (GCTs) constitute diverse neoplasms arising in the gonads or extragonadal locations. Testicular GCTs (TGCTs) are the predominant solid tumors in adolescents and young men. Despite cisplatin serving as the primary therapeutic intervention for TGCTs, 10‑20% of patients with advanced disease demonstrate resistance to cisplatin‑based chemotherapy, and epithelial‑mesenchymal transition (EMT) is a potential contributor to this resistance. EMT is regulated by various factors, including the snail family transcriptional repressor 2 (<i>SLUG</i>) transcriptional factor, and, to the best of our knowledge, remains unexplored within TGCTs. Therefore, the present study investigated the EMT transcription factor <i>SLUG</i> in TGCTs. <i>In silico</i> analyses were performed to investigate the expression of EMT markers in TGCTs. In addition, a cisplatin‑resistant model for TGCTs was developed using the NTERA‑2 cell line, and a mouse model was also established. Subsequently, EMT was assessed both <i>in vitro</i> and <i>in vivo</i> within the cisplatin‑resistant models using quantitative PCR and western blot analyses. The results of the <i>in silico</i> analysis showed that the different histologies exhibited distinct expression profiles for EMT markers. Seminomas exhibited a lower expression of EMT markers, whereas embryonal carcinomas and mixed GCT demonstrated high expression. Notably, patients with lower <i>SLUG</i> expression had longer median progression‑free survival (46.4 months vs. 28.0 months, P=0.022). In the <i>in vitro</i> analysis, EMT‑associated genes [fibronectin; vimentin (<i>VIM</i>); actin, α2, smooth muscle; collagen type I α1; transforming growth factor‑β1; and <i>SLUG</i>] were upregulated in the cisplatin‑resistant NTERA‑2 (NTERA‑2R) cell line after 72 h of cisplatin treatment. Consistent with this finding, the NTERA‑2R mouse model demonstrated a significant upregulation in the expression levels of VIM and SLUG. In conclusion, the present findings suggested that <i>SLUG</i> may serve a crucial role in connecting EMT with the development of cisplatin resistance, and targeting <i>SLUG</i> may be a putative therapeutic strategy to mitigate cisplatin resistance.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular senescence: A new perspective on the suppression of periodontitis (Review).","authors":"Xue-Jing Lin, Qing Yuan, Jie Zhou, Yu-Lei Dong, Diwas Sunchuri, Zhu-Ling Guo","doi":"10.3892/mmr.2024.13362","DOIUrl":"10.3892/mmr.2024.13362","url":null,"abstract":"<p><p>Cellular senescence, characterized by cell cycle arrest, can result in tissue dysfunction when senescent cells persist and accumulate. Periodontitis, a chronic inflammatory condition caused by the interaction between bacteria and the immune system of the host, primarily manifests as damage to periodontal tissues. Aging and inflammation are interlinked processes that exacerbate each other. The progression of localized chronic periodontal inflammation is often accelerated in conjunction with tissue and organ aging. The presence of senescent cells and release of inflammatory cytokines, immune modulators, growth factors and proteases that are associated with the senescence‑associated secretory phenotype contribute to the deterioration of periodontal tissues. The present review aimed to elucidate the mechanisms of cellular senescence and its potential impact on periodontitis, offering novel insights for modulating the inflammatory microenvironment of periodontal tissues.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stigmasterol exerts antiglioma effects by regulating lipid metabolism.","authors":"Ting Wei, Ruichun Li, Shiwen Guo, Chen Liang","doi":"10.3892/mmr.2024.13351","DOIUrl":"10.3892/mmr.2024.13351","url":null,"abstract":"<p><p>Stigmasterol is a sterol compound found in various traditional Chinese medicines; however, its effects on glioma remain unclear. The present study aimed to investigate the effects of stigmasterol on the biological behaviors of glioblastoma (GBM) cells and to explore the underlying mechanisms. <i>In vitro</i> experiments assessed its effects on GBM cell proliferation, apoptosis, cell cycle progression, invasion, migration and vasculogenic mimicry (VM). The potential targets for stigmasterol in treating GBM were identified using databases and Venn diagram analysis, followed by enrichment analysis using R language. A prognostic model related to the target genes of stigmasterol was developed through univariate Cox regression and least absolute shrinkage and selection operator analyses. Stigmasterol was found to suppress the proliferation of GBM cells in a dose‑ and time‑dependent manner, to induce apoptosis, and to inhibit invasion, migration and VM formation. Additionally, 31 potential targets of stigmasterol were identified, linked to lipid metabolism and the G protein‑coupled receptor signaling pathway. Lipid metabolism assays revealed that stigmasterol significantly reduced free fatty acids and total cholesterol levels. Furthermore, two prognosis‑related target genes, fatty acid binding protein 5 and α‑1B adrenergic receptor, were selected, and the prognostic model effectively predicted GBM outcomes. Moreover, molecular docking revealed strong binding affinities between stigmasterol and the target proteins. Overall, these findings suggested that stigmasterol may exert anti‑glioma effects, which could be potentially mediated through the regulation of lipid metabolism.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] MYCN‑amplified neuroblastoma cell‑derived exosomal miR‑17‑5p promotes proliferation and migration of non‑MYCN amplified cells.","authors":"Weiming Chen, Xiwei Hao, Binyi Yang, Yuezhen Zhang, Lingyun Sun, Yanan Hua, Li Yang, Jiabin Yu, Jing Zhao, Lin Hou, Hongting Lu","doi":"10.3892/mmr.2024.13349","DOIUrl":"10.3892/mmr.2024.13349","url":null,"abstract":"<p><p>Following the publication of this article, an interested reader drew to the authors' attention that the forward and reverse primer sequences written for GAPDH in Table I on p. 3 were incorrect. Upon requesting an explanation of these errors from the authors, they realized that these sequences had been written incorrectly in the paper: The sequence of the forward primer in Table I should have been written as 5'‑CAG GAGGCATTGCTGATGAT‑3', and the reverse primer should have been written as 5'‑GAAGGCTGGGGCTCATTT‑3'. The Editorial Office also requested seeing proof of purchase of the primers used in this study from the authors. The authors are grateful to the Editor of <i>Molecular Medicine Reports</i> for allowing them the opportunity to publish this corrigendum, and all the authors agree with its publication. The authors also regret the inconvenience that these mistakes have caused. [Molecular Medicine Reports 23: 245, 2021; DOI: 10.3892/mmr.2021.11884].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mild therapeutic hypothermic protection activates the PI3K/AKT signaling pathway to inhibit TRPM7 and suppress ferroptosis induced by myocardial ischemia‑reperfusion injury.","authors":"Yaqi Li, Yixuan Chen, Peng Yu, Deju Zhang, Xiaoyi Tang, Zicheng Zhu, Fan Xiao, Wei Deng, Yang Liu, Zhaoying Tan, Jing Zhang, Shuchun Yu","doi":"10.3892/mmr.2024.13345","DOIUrl":"10.3892/mmr.2024.13345","url":null,"abstract":"<p><p>The present study aimed to investigate the role of PI3K‑mediated ferroptosis signaling induced by mild therapeutic hypothermia (MTH), which was defined as a temperature of 34˚C, in protecting against myocardial ischemia-reperfusion (I/R) injury (MIRI). To meet this aim, H9C2 cells underwent hypoxia‑reperfusion (H/R) and/or MTH. The MTT assay was used to assess cell viability, cytotoxicity was measured using a lactate dehydrogenase cytotoxicity assay, and Annexin V‑FITC/PI flow cytometric analysis was used to analyze early and late cell apoptosis. In addition, 84 healthy adult male Sprague‑Dawley rats were randomly divided into seven groups (n=12), and underwent I/R and various treatments. Hemodynamics were monitored, and the levels of myocardial injury marker enzymes and oxidative stress markers in myocardial tissue were measured using ELISA. The expression levels of PI3K, AKT, transient receptor potential cation channel subfamily M member 7 (TRPM7), glutathione peroxidase 4 (GPX4) and acyl‑CoA synthetase long chain family member 4 (ACSL4) in animals and cells were measured using western blot analysis. These experiments revealed that MTH could effectively reduce myocardial infarct size, improve hemodynamic performance following MIRI and suppress myocardial apoptosis, thereby contributing to the recovery from H/R injury. Mechanistically, MTH was revealed to be able to activate the PI3K/AKT signaling pathway in cells, upregulating GPX4, and downregulating the expression levels of TRPM7 and ACSL4. Treatment with 2‑aminoethoxydiphenyl borate (an inhibitor of TRPM7) could further strengthen the myocardial protective effects of MTH, whereas treatment with erastin (promoter of ferroptosis) and wortmannin (inhibitor of PI3K) led to the effective elimination of the myocardial protective effects of MTH. Compared with in the I/R group, the PI3K/AKT activation level and the expression levels of GPX4 were both significantly increased, whereas the expression levels of TRPM7 and ACSL4 were significantly decreased in the I/R + MTH group. Taken together, the results of the present study indicated that MTH may activate the PI3K/AKT signaling pathway to inhibit TRPM7 and suppress ferroptosis induced by MIRI.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyphyllin II inhibits breast cancer cell proliferation via the PI3K/Akt signaling pathway.","authors":"Weiwei Miao, Zhixiong Wang, Jianwen Gao, Yuko Ohno","doi":"10.3892/mmr.2024.13348","DOIUrl":"10.3892/mmr.2024.13348","url":null,"abstract":"<p><p>Paridis Rhizoma saponins (PRS) are significant components of Rhizoma Paridis and have inhibitory effects on various tumors, such as bladder, breast, liver and colon cancer. Polyphyllin II (PPII), one of the PRS, has an unclear effect on breast cancer. The present study aimed to explore the effect and mechanism of PPII in breast cancer. A network pharmacology approach was employed to predict the core components and breast cancer‑related targets of PRS. Moreover, a xenograft tumor model was established to determine the anti‑breast cancer effect of PPII <i>in vivo</i>. The viability of MDA‑MB‑231 cells was determined by a Cell Counting Kit‑8 assay. Apoptosis was analyzed using annexin V/PI double staining. Additionally, Transwell and scratch assays were performed to evaluate invasion and migration. The potential mechanism was predicted by Kyoto Encyclopedia of Genes and Genomes enrichment analysis and molecular docking analysis and verified by western blot analysis. The effect of PPII on aerobic glycolysis in breast cancer cells was detected by lactic acid and pyruvate kits and Western blotting of glycolytic rate‑limiting enzymes. Network pharmacology analysis revealed 26 core targets involved in breast cancer and that PPII was the core active component of PRS. The in vivo studies showed that PPII could inhibit the growth of breast cancer in mice. <i>In vitro</i> experiments confirmed that PPII induced cancer cell apoptosis and inhibited invasion and migration. Furthermore, PPII was capable of suppressing the expression of key proteins in the PI3K/Akt signaling pathway, reducing the generation of aerobic glycolytic products, and diminishing the protein expression levels of hexokinase 2 and pyruvate kinase M2. The results indicated that PPII inhibited aerobic glycolysis in breast cancer cells through the PI3K/Akt signaling pathway, thereby inhibiting breast cancer growth.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoplasmic reticulum stress induces renal fibrosis in high‑fat diet mice via the TGF‑β/SMAD pathway.","authors":"Zhidan Mu, Bin Li, Mingyang Chen, Chen Liang, Wei Gu, Juan Su","doi":"10.3892/mmr.2024.13360","DOIUrl":"10.3892/mmr.2024.13360","url":null,"abstract":"<p><p>The aim of the present study was to investigate the role and mechanism of endoplasmic reticulum stress (ERS) in kidney injury caused by high‑fat diet (HFD). An obese mouse model was established via HFD feeding and intervention was performed by intraperitoneal injection of the ERS inhibitor salubrinal (Sal). Changes in the body and kidney weight and serum biochemical indices of the mice were determined. Hematoxylin and eosin and Masson staining were used to observe the pathological changes of renal tissues. Reverse transcription‑quantitative PCR and western blotting were used to observe the expression of ERS‑related proteins and TGF‑β/SMAD pathway‑related proteins. Immunohistochemistry was employed to explore the distribution of these proteins. Compared with those in the control group, the weight gain, lipid metabolism disorders and deterioration of renal function in the model group were greater. Malondialdehyde was elevated and superoxide dismutase was decreased in renal tissues. The mRNA and protein levels of TGF‑β1, SMAD2/3, α‑smooth muscle actin, collagen I, glucose‑regulated protein 78 and C/EBP‑homologous protein were markedly elevated, whereas SMAD7 was markedly decreased. Sal markedly inhibited the aforementioned effects. This investigation revealed a link between ERS and renal injury caused by HFD. ERS in HFD‑fed mice triggers renal fibrosis through the TGF‑β/SMAD pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LPS‑mediated adaptation accelerates ecto‑MSCs differentiation into osteoblasts.","authors":"Demin Lv, Bingxia Li, Zhen Liu, Qing Zhang, Sucheng Cao, Yanlong Xu, Zheng Zhang","doi":"10.3892/mmr.2024.13365","DOIUrl":"10.3892/mmr.2024.13365","url":null,"abstract":"<p><p>Addressing the repair and regeneration of large bone defects poses significant challenges in bone tissue engineering. Despite the abundant evidence demonstrating the positive role of MSCs in osteogenesis, their limited osteogenic differentiation ability still needs to be improved. The present study used lipopolysaccharide (LPS) to enhance the osteogenic properties of ecto‑mesenchymal stem cells (EMSCs). Human nasal respiratory mucosa‑derived EMSCs were cultured on plates and stimulated with LPS for 5 days prior to undergoing osteogenic differentiation. The findings revealed that LPS effectively stimulated the osteogenic differentiation capacity of EMSCs, as evidenced by heightened alkaline phosphatase activity, elevated expression levels of osteogenic‑related proteins and enhanced mineralization of EMSCs. The present study also demonstrated that the augmentation occurred due to increased IL‑10 levels, although it was not solely attributable to this factor. Together, the findings illustrated that the LPS‑mediated adaptation of EMSCs is an active process driving osteogenic differentiation and could be a novel strategy for bone regeneration.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] LncRNA HOTAIR controls the expression of Rab22a by sponging miR‑373 in ovarian cancer.","authors":"Zhongbao Zhang, Jiajing Cheng, Yi Wu, Jin Qiu, Yi Sun, Xiaowen Tong","doi":"10.3892/mmr.2024.13346","DOIUrl":"10.3892/mmr.2024.13346","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the cell apoptotic data shown in Fig. 3C and the Hoeschst 33342‑stained images in Fig. 3D on p. 2468, and certain of the scratch‑wound assay data shown in Fig. 5E on p. 2470 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to <i>Molecular Medicine Reports</i>, or were submitted for publication at around the same time. Owing to the fact that some of the abovementioned data had already apparently been published previously, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 14: 2465‑2472, 2016; DOI: 10.3892/mmr.2016.5572].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}