International journal of molecular medicine最新文献

{"title":"Multiple roles and mechanisms of MUC6 in cancer (Review).","authors":"Xin Luo, Xiao Fu, Ying Xiong, Ping Xiao","doi":"10.3892/ijmm.2025.5629","DOIUrl":"10.3892/ijmm.2025.5629","url":null,"abstract":"<p><p>Mucin 6 (MUC6), primarily expressed in the gastrointestinal (GI) epithelium, is a member of the mucin family characterized by a protein backbone with extensive glycosylation, playing a crucial role in preserving epithelial barrier integrity. Accumulating evidence indicates that MUC6 glycosylation contributes significantly to cancer development, diagnosis, therapy and prognosis‑particularly in GI malignancies such as gastric, pancreatic and colorectal cancers. In the present review, current findings on the multifaceted roles of MUC6 across various cancers were comprehensively summarize. For instance, loss of MUC6 expression is frequently associated with gastric cancer risk, while its upregulation may serve as a valuable biomarker in prostate cancer biopsy, aiding in early detection. Additionally, the identification of MUC6‑Tn glycoforms offers promising avenues for novel therapeutic strategies. The distinctive tandem repeat polymorphisms within the MUC6 gene further suggest its potential utility in assessing cancer susceptibility based on allele length variation. These insights underscore the relevance of MUC6 in both mechanistic research and clinical oncology. Although preliminary data are encouraging, large‑scale, multicenter studies are necessary to fully validate the clinical application of MUC6 as a biomarker for cancer staging and prognosis. Finally, the present review outlines future directions for exploring MUC6 in the context of cancer therapy development.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000552","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] Μolecular impact of bone morphogenetic protein 7, on lung cancer cells and its clinical significance.","authors":"Yinan Liu, Jinfeng Chen, Yue Yang, Lijian Zhang, Wen G Jiang","doi":"10.3892/ijmm.2025.5585","DOIUrl":"10.3892/ijmm.2025.5585","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that, for the electrophoretic blots shown in Fig. 3A‑a, the data shown for the BMP7 and GAPDH bands were strikingly similar, such that it appeared that the same data had been included in this figure part to show the results from the differently performed experiments. The authors were able to re‑examine their original data, and realized that the BMP7 bands had inadvertently been included in this figure twice. The revised version of Fig. 3, now incorporating the correct data for the GAPDH bands in Fig. 3A‑a, is shown on the next page. The authors can confirm that the error made in asembling this figure did not have a significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 29: 1016‑1024 2012; DOI: 10.3892/ijmm.2012.948].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667605","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":"Mechanism of action and therapeutic potential of S100A8/A9 in neuroinflammation and cognitive impairment: From molecular target to clinical application (Review).","authors":"Xilong Guan, Linan Zha, Xiaoling Zhu, Xiuqin Rao, Xiangfei Huang, Yanhong Xiong, Youwei Guo, Mojiao Zhang, Dongshan Zhou, Qikun Tu, Jianhang Wu, Xifeng Wang, Fuzhou Hua, Jing Xu","doi":"10.3892/ijmm.2025.5588","DOIUrl":"10.3892/ijmm.2025.5588","url":null,"abstract":"<p><p>The complex of proteins S100A8/A9 has been recognized as a major initiator of cognitive disorder onset, including, but not restricted to, neuroinflammation. Cognitive impairment or decline in memory, attention and executive function has been on the rise and is a major public health priority. Several neurological conditions that affect the brain and cognitive processes, including central nervous system diseases such as Alzheimer's disease and stroke, and systemic diseases, such as sepsis and systemic lupus erythematosus, are associated with S100A8/A9. Experiments have progressively demonstrated that S100A8/A9 plays a role in cognitive decline, as it regulates cognitive domains, including sleep, learning, memory, and emotion control, via several mechanisms. In this review, a critical overview of the role of S100A8/A9 in the treatment of neurocognitive diseases is provided, including the regulation of brain function and the pathogenesis of diseases, and potential novel therapies are suggested. It is necessary to study S100A8/A9 alone as an alternative marker for the diagnosis and treatment of neurocognitive diseases, and in line with the requirements of therapy for cognitive impairment. As S100A8/A9 research continues, the understanding and treatment of neurocognitive diseases may improve.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667610","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":"Histone deacetylase 4: A therapeutic target for cardiovascular diseases (Review).","authors":"Xiaotong Ma, Ran Wei, Anni Song, Xinyi Zhang, Jianpeng Zou, Shijie Hao","doi":"10.3892/ijmm.2025.5599","DOIUrl":"10.3892/ijmm.2025.5599","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) is a major global health threat, as its incidence and mortality rates continue to rise, highlighting the urgent need for effective therapeutic strategies. Histone deacetylase 4 (HDAC4), a member of class IIa HDACs, has attracted increasing attention in recent years for its role in CVD. Studies have shown that HDAC4 can influence the development and progression of CVD such as cardiac hypertrophy, hypertension and atherosclerosis by regulating key pathophysiological processes including inflammation, fibrosis and apoptosis. The present review focuses on the functional roles of HDAC4 in CVD and examines the effects of pharmacological agents and physical exercise on its expression. Future research should further elucidate the molecular mechanisms underlying HDAC4's involvement in CVD to provide new theoretical foundations for clinical diagnosis and treatment.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760056","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":"Pyroptosis in gastric mucosal injury‑related diseases (Review).","authors":"Bei Ji, Zhiyuan Ma, Shuhui Liu, Shun Yao, Kenichi Mizuno, Shuji Terai, Biguang Tuo, Taolang Li, Xuemei Liu","doi":"10.3892/ijmm.2025.5606","DOIUrl":"10.3892/ijmm.2025.5606","url":null,"abstract":"<p><p>Gastric mucosal epithelial cells, immune cells and signaling molecules constitute the innate and adaptive immune systems of the gastric mucosa, working together to maintain its integrity. Once the balance is disrupted, gastric mucosal diseases may occur. Pyroptosis, as a unique inflammatory programmed cell death mechanism, participates in the dynamic balance between innate and adaptive immunity by identifying and responding to damage factors, and participating in the maturation and release process of inflammatory factors. Pyroptosis is involved in the association of gastric mucosal resistance with microbial invasion and endogenous damage. By releasing inflammatory factors, the immune environment of the gastric mucosa is reshaped, thereby affecting repair mechanisms and the specific direction of cell differentiation. The present review summarizes the important role of pyroptosis in focal and diffuse gastric mucosal injury. The review aims to provide a novel theoretical basis for the optimization of prevention strategies and treatment plans for current gastric mucosal diseases, and proposes a new option for the scientific management of these diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799039","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":"Macrophage migration inhibitory factor: Exploring physiological roles and comparing health benefits against oncogenic and autoimmune risks (Review).","authors":"Gustavo Camacho Meza, Guadalupe Avalos Navarro, Ulises De La Cruz Mosso, Ramiro Ramírez Patiño, Jose Francisco Muñoz Valle, Luis Alberto Bautista Herrera","doi":"10.3892/ijmm.2025.5590","DOIUrl":"10.3892/ijmm.2025.5590","url":null,"abstract":"<p><p>Macrophage migration inhibitory factor (MIF), a multifunctional cytokine that plays a central role in immune regulation and tissue homeostasis, is expressed by nearly all cell types in the body. Beyond its well‑established pro‑inflammatory functions, MIF also exerts protective effects in several physiological processes. MIF enhances immune defense by activating macrophages, promoting cytokine release and supporting efficient antigen presentation. Additionally, MIF contributes to tissue repair, neuroprotection, cardiac function and metabolic regulation, facilitating epithelial healing, maintaining redox balance and modulating insulin secretion. MIF signals through multiple receptors, including CD74, CD44, CXC motif chemokine receptor (CXCR)2, CXCR4 and CXCR7, enabling it to act across a wide range of cell types. This complex signaling network allows MIF to function as both a mediator of homeostasis and a driver of pathology, depending on the biological context. Elevated MIF levels and polymorphisms such as ‑794 CATT5‑8 and ‑173G>C have been associated with increased susceptibility to and the severity of autoimmune disorders (such as systemic lupus erythematosus, multiple sclerosis and rheumatoid arthritis), cancer (such as breast, lung and colorectal cancer) and other inflammatory diseases. MIF promotes tumor progression, immune evasion and glucocorticoid resistance, positioning it as a potential biomarker and therapeutic target. Therapeutic strategies targeting MIF, such as small‑molecule inhibitors, receptor antagonists and proteolysis‑targeting chimeras, have shown promise in preclinical studies. However, translating these strategies into clinical therapies requires a deeper understanding of the tissue‑specific functions of MIF and the long‑term consequences of its modulation. Future research should focus on elucidating the mechanisms underlying the dual roles of MIF in health and disease, the impact of genetic variations and the development of targeted interventions that preserve its protective functions while minimizing its pathogenic potential. Such insights will be essential for advancing MIF‑based therapies in precision medicine.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12306601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667609","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":"Dulaglutide markedly prevents peritoneal fibrosis in a rodent model of chronic kidney disease: Insights into the pathogenesis.","authors":"Chih-Chao Yang, Ya Yue, Yi-Ting Wang, John Y Chiang, Ben-Chung Cheng, Tsuen-Wei Hsu, Yi-Ling Chen, Yi-Chen Li, Hon-Kan Yip","doi":"10.3892/ijmm.2025.5592","DOIUrl":"10.3892/ijmm.2025.5592","url":null,"abstract":"<p><p>Peritoneal fibrosis (PF) is a major complication of long-term peritoneal dialysis, leading to ultrafiltration failure and technique dropout, highlighting the urgent need for therapies that can preserve peritoneal membrane function and longevity. The present study evaluated the effectiveness of dulaglutide in preserving the functional integrity and durability of the peritoneum while inhibiting PF. <i>In vitro</i> Met-5A cells showed significant upregulation of inflammatory, oxidative stress, intracellular and mitochondrial reactive oxygen species (ROS), fibrotic, intracellular cytoskeletal, apoptotic and epithelial-mesenchymal transition (EMT) biomarkers, and dipeptidyl peptidase 4 (DPP4), following stimulation with a uremic toxin (p-Cresol), PF inducer [chlorhexidine gluconate (CG)] or endotoxin [lipopolysaccharide (LPS)]. Notably, these effects were significantly suppressed by dulaglutide or TGF-β/DPP4 double silencing. Furthermore, cell viability and glucagon-like peptide 1 (GLP-1) expression displayed an opposite pattern to ROS among the groups. Sprague-Dawley rats were divided into the following groups: i) Sham control (SC); ii) chronic kidney disease (CKD); iii) CKD + CG (mimicking renal failure and PF); and iv) CKD + CG + dulaglutide, and were euthanized by day 42. At this time point, the highest levels of peritoneal protein expression levels of oxidative stress (NOX-1, NOX-2 and DPP4), inflammation (NF-κB and TNF-α), angiogenesis (CD31 and von Willebrand factor) and EMT (TGF-β, Snail, β-catenin, vimentin, phosphorylated-Smad3, α-smooth muscle actin, collagen I, N-cadherin and fibronectin) factors; and cellular expression levels of fibrosis and inflammation markers, were observed in the CKD + CG group, the lowest were detected in the SC group, and the levels were significantly reduced in the CKD + CG + dulaglutide group compared with those in the CKD group. Furthermore, the expression levels of antioxidant proteins (nuclear factor erythroid 2-related factor 2, NAD(P)H quinone oxidoreductase 1 and GLP-1 receptor) exhibited an opposite trend to ROS-associated proteins among the groups. Additional Sprague-Dawley rats were categorized into the following groups: i) SC; ii) LPS-induced peritonitis; iii) LPS-induced peritonitis + dulaglutide, and were euthanized by day 5 after peritonitis induction. At this time point, flow cytometry revealed significantly increased levels of inflammatory cells (CD11b/c⁺, myeloperoxidase⁺ and Ly6G⁺ cells) in the circulation and abdominal fluid, and increased peritoneal permeability in the LPS-induced peritonitis group compared with those in the SC group; these levels were significantly reversed in the LPS-induced peritonitis + dulaglutide group. In conclusion, dulaglutide may effectively maintain peritoneal integrity primarily by suppressing inflammation, oxidative stress, EMT and fibrosis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12306598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707443","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":"Kirenol relieves rheumatoid arthritis by targeting the TWEAK/Fn14 pathway.","authors":"Zixin Chen, Jinxuan Wang, Lijuan Xiao, Zhihui Chen, Wenchuan Luo, Wen Xu, Ya Lin, Mei Huang, Yuqian Zhang, Yinghao Wang, Yaping Chen, Lihong Nan","doi":"10.3892/ijmm.2025.5586","DOIUrl":"10.3892/ijmm.2025.5586","url":null,"abstract":"<p><p>Fibroblast‑like synoviocytes (FLSs) are the primary drivers of synovial tissue hyperplasia in rheumatoid arthritis (RA). Activation of the tumor necrosis factor‑like weak inducer of apoptosis (TWEAK)/fibroblast growth factor‑inducible immediate‑early response protein 14 (Fn14) pathway significantly contributes to the pathogenesis of RA. Kirenol (Kir), a compound with anti‑inflammatory and antirheumatic properties, has an unclear mechanism of action. To comprehensively investigate the effects and potential mechanisms of Kir on RA, the present study employed both an <i>in vitro</i> model of transforming growth factor‑β1 (TGF‑β1)‑induced human fibroblast‑like MH7A synoviocytes proliferation and an <i>in vivo</i> collagen‑induced arthritis (CIA) rat model. The effects of Kir on synovial fibroblasts were detected via flow cytometry, ELISA, hematoxylin and eosin staining, safranin‑O/fast green staining, immunohistochemistry, immunofluorescence and western blotting. Kir ameliorated pathological damage in the synovial tissue of CIA rats, suppressed rheumatoid factor production, regulated the T helper 17 cells/regulatory T cell balance and mitigated joint inflammation and swelling. Additionally, Kir markedly downregulated the protein levels of the TWEAK/Fn14 pathway in synovial tissue. Surface plasmon resonance demonstrated that Kir could specifically bind to Fn14. Kir significantly suppressed the TGF‑β1‑mediated aberrant proliferation and migration of MH7A cells. However, the overexpression of Fn14 reversed the inhibitory effects of Kir on the abnormal proliferation and migration of cells, as did the activation of the TWEAK/Fn14 pathway. These results suggest that Kir possesses anti‑RA properties by inhibiting abnormal immune‑inflammatory responses, as well as synovial cell proliferation and migration. These effects of Kir may be linked to a decrease in the activity of the TWEAK/Fn14 pathway.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667608","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":"Secretion of specific metabolites and changes in miRNA expression in murine osteoblastic cells exposed <i>in vitro</i> to α‑radiation.","authors":"Satoru Monzen, Yota Tatara, Mitsuru Chiba, Yasushi Mariya, Andrzej Wojcik","doi":"10.3892/ijmm.2025.5602","DOIUrl":"10.3892/ijmm.2025.5602","url":null,"abstract":"<p><p>Osteoblastic cells (OBCs) in bone marrow (BM) support hematopoietic stem/progenitor cells (HSPCs) by forming a regulatory niche through cytokine and metabolite secretion. Targeted α‑emitting radionuclide therapy, such as radium‑223 dichloride (²²³RaCl₂), is effective in treating bone metastases but frequently causes unpredictable hematologic toxicities. The underlying mechanism remains unclear. The present study hypothesized that α‑radiation alters the OBC secretome and miRNA expression, thereby modulating the BM microenvironment and influencing therapy response. The present study aimed to characterize proteomic, lipidomic and miRNA expression profiles in OBCs following α‑radiation exposure. Primary murine BM cells were differentiated into OBCs and irradiated with 0‑1 Gy of α‑radiation using a ²⁴¹Am source. Mass spectrometry was used to analyze intracellular proteins and lipids and miRNA expression was assessed by microarray analysis. Kyoto Encyclopedia of Genes and Genomes pathway enrichment was performed using OmicsNet 2.0. α‑radiation markedly reduced OBC clonogenic survival and induced specific molecular alterations. α total of six proteins and several lipid species, particularly from the phosphatidylcholine family, showed significant alterations. miRNAs including miR‑1895, miR‑370‑3p and miR‑188‑5p were downregulated. Enrichment analysis revealed involvement in transcriptional regulation, apoptosis, glycerophospholipid metabolism and cytokine signaling. In conclusion, α‑radiation induced distinct proteomic, lipidomic and miRNA changes in OBCs, potentially affecting BM radiosensitivity. These molecules may serve as candidate biomarkers for predicting individual susceptibility to α‑emitting radionuclide therapy.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799040","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] Epithelial‑mesenchymal transition is necessary for acquired resistance to cisplatin and increases the metastatic potential of nasopharyngeal carcinoma cells.","authors":"Pei Zhang, Hao Liu, Fei Xia, Qian Wen Zhang, Yuan Yuan Zhang, Qing Zhao, Zhen Hua Chao, Zhi Wen Jiang, Chen Chen Jiang","doi":"10.3892/ijmm.2025.5591","DOIUrl":"10.3892/ijmm.2025.5591","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that Figs. 3B and 4B contained western blot data (specifically, the MMP‑9 and Vimentin western blots in Figs. 3B and 4B, respectively) that were more similar than expected. Moreover, further strikingly similar data were also identified examining the western blot data within Fig. 4B and 4D, and also comparing the western blots in Figs. 1D, 3B, 4B and 4D with data featured in an article in the journal <i>Oncotarget</i> that was published subsequently to the above article, but which featured the first author (Pei Zhang) as an author in common. The authors were able to re‑examine their original data (which were also presented to the Editorial Office), and confirmed that the Vimentin data in Fig. 4B and the ZEB1 data in Fig. 4D were the same western bands as those featured for the MMP‑9 data in Fig. 3B and the Fibronectin data in Fig. 4B, respectively. These errors were made during the assembly of Fig. 4 (the data for MMP‑9 and Fibronectin were inadvertently duplicated in the figure). The corrected version of Fig. 4, now displaying the accurate experimental data for the Vimentin (Fig. 4B) and ZEB1 (Fig. 4D) blots in the CNE2Z and CNE2Z/DDP groups, is shown on the next page. Furthermore, regarding the issue of image duplication comparing between the above article published in 2014 and the one published in <i>Oncotarget</i> in 2015, the authors will contact the <i>Oncotarget</i> journal to handle the necessary corrections. The authors can confirm that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 33: 151‑159, 2014; DOI: 10.3892/ijmm.2013.1538].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12306597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707335","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}