Molecular medicine reports最新文献

{"title":"Role of COUP‑TFII in cardiovascular diseases and colorectal cancer: Insights into the molecular mechanisms and clinical relevance (Review).","authors":"Tae-Ho Park, Sang-Heum Han, Jun-Gi Cho, Su-Jeong Park, Jin-Yeong Han, Joo-In Park","doi":"10.3892/mmr.2025.13631","DOIUrl":"https://doi.org/10.3892/mmr.2025.13631","url":null,"abstract":"<p><p>Chicken ovalbumin upstream promoter‑transcription factor II (COUP‑TFII), also known as nuclear receptor subfamily 2 group F member 2, is an orphan nuclear receptor that controls various biological processes, including development, angiogenesis, metabolism and tissue homeostasis. Structurally, COUP‑TFII comprises a DNA‑binding domain and a ligand‑binding domain, facilitating its interaction with various signaling pathways, and thereby exerting diverse biological effects. Alterations of the expression or transcriptional activity of COUP‑TFII are associated with various diseases, including cardiovascular diseases (CVDs) and different types of cancer such as colorectal cancer (CRC). In the context of CVDs, COUP‑TFII serves a key role in the development and function of the vascular system. Dysregulation of COUP‑TFII leads to aberrant angiogenesis and vascular remodeling, contributing to the pathogenesis of various CVDs. In CRC, COUP‑TFII acts as either a tumor suppressor or a tumor promoter, depending on the cellular context. The present review explores the structure and regulatory mechanisms of COUP‑TFII, its functions and molecular mechanisms in CVDs and CRC, and its emerging role in linking these diseases, offering insights into potential treatments and future research directions.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model.","authors":"Jue Wang, Dong Han, Miao Sun, Juan Feng","doi":"10.3892/mmr.2025.13641","DOIUrl":"https://doi.org/10.3892/mmr.2025.13641","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, the authors drew to the Editor's attention that matching HMGB1 bands featured in Figs. 4 and 5 had inadvertently been included in these figures twice; moreover, the GAPDH western blot controls featured in Fig. 3 had also been selected incorrectly. Revised versions of Fig. 3, 4 and 5, now featuring the corrected GAPDH western blots in Fig. 3, replacement data for the Beclin1 blots and the GAPDH blots in Fig. 4B and the HGMB‑1 bands in Fig. 4F, and replacement blots for the free beclin‑1 and HMGB‑1 bands in Fig. 5, are shown on the next three pages. Note that these errors did not adversely affect either the results or the overall conclusions reported in this study. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>Molecular Medicine Reports</i> for allowing them the opportunity to publish this. They also wish to apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 14: 4162‑4172, 2016; DOI: 10.3892/mmr.2016.5747].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] Expression and clinical significance of hypoxia‑inducible factor 1α, Snail and E‑cadherin in human ovarian cancer cell lines.","authors":"Yan Zhang, Nina Fan, Jing Yang","doi":"10.3892/mmr.2025.13638","DOIUrl":"https://doi.org/10.3892/mmr.2025.13638","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the invasion assay data shown in Fig. 1 on p. 3395 had apparently already been submitted in different form to the journal <i>OncoTarget</i> in a paper written by different authors at different research institutes. In view of the fact that the abovementioned data had apparently already been submitted for publication prior to their receipt at <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should now 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 12: 3393‑3399, 2015; DOI: 10.3892/mmr.2015.3786].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual role of hydrogen sulfide in the tumor microenvironment of prostate cancer (Review).","authors":"Hua Luo","doi":"10.3892/mmr.2025.13637","DOIUrl":"https://doi.org/10.3892/mmr.2025.13637","url":null,"abstract":"<p><p>Tumor microenvironment (TME) dynamics and the critical dual role of hydrogen sulfide (H2S) in prostate cancer (PCa) biology are discussed in the present review. PCa remains one of the most prevalent malignancies in men, with advanced castration‑resistant PCa presenting substantial therapeutic challenges. H2S, an endogenous gaseous signaling molecule, is a key regulator of biological processes, including immune modulation, cell proliferation and apoptosis, during tumor progression. H2S exhibits paradoxical effects in PCa by promoting tumorigenesis and exerting context‑dependent antitumor activity. H2S mediates these outcomes through key signaling pathways, including the PI3K/AKT and MAPK/ERK pathways, which regulate tumor cell survival and metastasis. The present review emphasizes how H2S regulates tumor cell dynamics and immune interactions in a concentration‑dependent manner within the TME, making it a promising therapeutic target to overcome resistance to conventional treatments. Future research should prioritize translating these findings into clinical strategies, particularly through the development of H2S‑modulating therapies tailored to the TME, offering potential for overcoming resistance in advanced PCa.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial‑endoplasmic reticulum crosstalk: Molecular mechanisms and implications for cardiovascular disease (Review).","authors":"Yue Liu, Xuejia Gong, Shasha Xing","doi":"10.3892/mmr.2025.13640","DOIUrl":"https://doi.org/10.3892/mmr.2025.13640","url":null,"abstract":"<p><p>Cardiovascular disease (CVD), which includes conditions such as coronary heart disease, hypertension, heart failure and diabetes cardiomyopathy, is a major cause of mortality among middle‑aged and elderly populations worldwide; however, there is a concerning trend of individuals of increasingly younger ages being affected. Despite extensive research and numerous treatments available, CVD remains a major health threat for middle‑aged and elderly individuals due to its complex causes and the effect of environmental and lifestyle factors. In recent years, the structural and functional abnormalities of mitochondria and endoplasmic reticulum (ER) organelles have been associated with CVD. In addition to the intrinsic role of organelles, the interaction between organelles, particularly the homeostasis imbalance between the mitochondria and the ER through the interaction of the mitochondria‑associated ER membrane (MAM), serves a key role in CVD, such as ischemia‑reperfusion, diabetic cardiomyopathy and heart failure. The main mechanism involves regulating lipid transport, calcium homeostasis, mitochondrial function, cell survival and death, as well as signal transduction. The present review summarized recent advancements in MAM research, elucidated key mechanisms that influence MAM homeostasis, highlighted its significance in cardiovascular health and disease and explored its potential as a therapeutic target for CVD, thereby providing a theoretical foundation for future research.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rev‑erbα: The circadian guardian against NLRP3‑driven liver fibrosis.","authors":"Junmin Wang, Yanping Wang, Liubing Lin, Wen Pei, Yong Li","doi":"10.3892/mmr.2025.13635","DOIUrl":"https://doi.org/10.3892/mmr.2025.13635","url":null,"abstract":"<p><p>Liver fibrosis is a pivotal pathological process in the progression of various chronic liver diseases toward cirrhosis, primarily driven by the activation of hepatic stellate cells. Recent studies have implicated dysregulation of circadian clock genes in the pathogenesis of hepatic disorders. The present investigation focused on the role of the circadian regulator nuclear receptor subfamily 1 group D member 1 (Rev‑erbα) in liver fibrosis and its mechanistic interplay with the NLR family domain containing protein 3 (NLRP3) inflammasome. A mouse model of liver fibrosis was established via carbon tetrachloride (CCl4) administration. The expression of Rev‑erbα was modulated pharmacologically using the agonist GSK4112 and the antagonist SR8278 to assess its impact on fibrogenesis. In parallel, lentiviral vectors were employed in <i>in vitro</i> studies to generate LX‑2 cell lines with Rev‑erbα overexpression or knockout. Transforming growth factor‑β1 (TGF‑β1) was applied to induce cellular activation, and subsequent effects on the NLRP3 inflammasome and its downstream mediators were analyzed. The extent of fibrosis and molecular alterations were evaluated using Masson's trichrome staining, Sirius Red staining, immunohistochemistry, western blotting and reverse transcription‑quantitative PCR. Rev‑erbα expression was significantly downregulated in both CCl4‑induced murine models and TGF‑β1‑activated LX‑2 cells. Pharmacological activation of Rev‑erbα attenuated hepatic fibrosis, evidenced by reduced collagen accumulation and suppression of fibrogenic markers (α‑smooth muscle actin, collagen 1 and TGF‑β1). By contrast, inhibition of Rev‑erbα exacerbated fibrotic responses. Mechanistically, Rev‑erbα activation inhibited NLRP3 inflammasome signaling and downstream pro‑inflammatory cytokines [interleukin (IL)‑18 and IL‑1β], underscoring its anti‑fibrotic function via NLRP3 pathway modulation. Rev‑erbα functions as a key negative regulator of hepatic fibrosis by suppressing NLRP3 inflammasome activation, representing a promising therapeutic target for the management of liver fibrosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of obesity and estrogen deficiency in non‑alcoholic fatty liver disease: Insights from a mouse model.","authors":"Aaron Afonso-Alí, Jano Dicroce-Giacobini, Silvia Teixido-Trujillo, Esteban Porrini, José Antonio Pérez-Pérez, Sonia García-Hernández, Sergio Luis-Lima, Beatriz Abrante-Pérez, Alberto Hernández-Bustabad, Nieves Guadalupe Acosta-González, Miriam Iglesias-Hernández, Laura Díaz-Martín, Covadonga Rodríguez-González, Manuel Hernández-Guerra, Ana Elena Rodríguez-Rodríguez","doi":"10.3892/mmr.2025.13629","DOIUrl":"https://doi.org/10.3892/mmr.2025.13629","url":null,"abstract":"<p><p>The prevalence of non‑alcoholic fatty liver disease (NAFLD) increases in post‑menopausal women, driven by obesity and metabolic syndrome (MS). However, the pathogenesis of this interaction remains poorly understood. The present study investigated the interplay between obesity, menopause and NAFLD in a C57BL6/J mouse model of diet‑induced obesity. The study included male and female animals, in which a subgroup of females underwent ovariectomy to simulate menopause. Mice were fed a high‑fat diet for 6 months which resulted in them becoming overweight, and developing hyperglycemia and insulin resistance. The present study analyzed liver histology, inflammatory markers and hepatic lipid profiles. All obese animals showed liver steatosis, hepatocyte ballooning and fibrosis. Sex‑related differences were observed, including: i) Obese male mice developed increased expression of inflammatory markers and altered lipid profile; ii) obese female mice exhibited less severe steatosis, hepatic inflammation and lipotoxicity, and iii) ovariectomized obese female mice exhibited exacerbated hepatic lipotoxicity and tissue damage. Ovariectomized obese female mice also had reduced triacylglycerol and cholesteryl ester levels, but increased levels of toxic intermediaries, such as free fatty acids, diacylglycerols and free cholesterol, elevated expression of NF‑κB in the liver and increased levels of serum transaminases, indicating liver damage. These findings suggested that estrogen may protect against NAFLD progression by regulating lipid droplet formation, especially in the context of insulin resistance. More studies in the field are clearly needed to achieve a complete understanding of these pathways, which may serve to improve current therapies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression, immunogenicity and clinical significance analysis of thyroid‑stimulating hormone receptor fusion proteins.","authors":"Xia Chen, Hui Chen","doi":"10.3892/mmr.2025.13639","DOIUrl":"https://doi.org/10.3892/mmr.2025.13639","url":null,"abstract":"<p><p>Thyroid function is regulated in a substantial manner by thyroid‑stimulating hormone receptor (TSHR), and aberrant alterations in thyroid function are triggered by the interaction of TSHR with its antibodies, thyroid‑stimulating hormone receptor antibodies (TRAb). The expression, immunogenicity and clinical significance of fusion proteins comprising different structural domains of TSHR were investigated. Fusion proteins containing several human TSHR (hTSHR) structural domains were created. <i>In vitro</i> experiments utilized these fusion proteins as antigens to specifically bind and analyze patient sera using an ELISA. To investigate the immunogenicity and clinical significance of various structural domains of TSHR, <i>in vivo</i> experiments included immunizing BALB/c mice with various fusion proteins of hTSHR, measuring serum autoantibodies, assessing thyroid function, performing histological examination and using flow cytometry to identify changes in T cell subsets. Three distinct hTSHR fusion protein fragments (hTSHR289, hTSHR290 and hTSHR410) were synthesized. The hTSHR290 fusion protein demonstrated the highest binding reaction with TRAb⁺ sera from patients with hypothyroidism, and the hTSHR289 fusion protein demonstrated considerable specific binding reactivity with stimulating antibodies, as observed in sera from patients with hyperthyroidism. Pathological alterations associated with hyperthyroidism were observed in mice in the hTSHR289 fusion protein group, while pathological changes associated with hypothyroidism were observed in mice in the hTSHR290 fusion protein group. Immunized BALB/c mice exhibited increased levels of CD4⁺ T cell subsets, and decreased levels of CD8⁺CD122⁺ and CD4⁺CD25⁺ T cell subsets. Fusion proteins of different structural domains of TSHR exhibited varying immunogenicity. The hTSHR289 fusion protein and hTSHR290 fusion protein prepared in the present study could serve as a basis for the development of ELISA kits for the detection of thyroid‑stimulating immunoglobulins and TSHR‑blocking antibodies. Fusion proteins of different structural domains of TSHR induced clinical symptoms of hyperthyroidism and hypothyroidism in mice. The present study provides a scientific basis for future studies on the etiology and mechanisms of autoimmune thyroid diseases, as well as the invention of novel methods for TRAb detection.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel tRNA‑derived small RNA, 5'tiRNA‑Gln‑TTG‑001, aggravates cardiomyocyte inflammatory injury through upregulation of CLIC4.","authors":"Jing Wang, Yingchun Yi, Bo Han, Li Zhang, Hailin Jia","doi":"10.3892/mmr.2025.13626","DOIUrl":"10.3892/mmr.2025.13626","url":null,"abstract":"<p><p>Acute myocarditis encompasses a spectrum of diseases characterized by ongoing inflammation and cardiomyocyte injury, lacking specific diagnostic biomarkers and effective therapies. Transfer RNA (tRNA)‑derived small RNAs (tsRNAs), formed by specific cleavage of tRNAs in response to certain stimuli, participate in diverse diseases; however, their involvement in myocarditis remains unclear. The present study aimed to investigate the role and mechanism of a novel tsRNA, 5'tRNA‑derived stress‑induced RNA (tiRNA)‑Gln‑TTG‑001, in myocarditis. Plasma samples were obtained from patients with acute myocarditis to examine the clinical significance of 5'tiRNA‑Gln‑TTG‑001. AC16 human cardiomyocytes treated with lipopolysaccharide to induce inflammatory responses were utilized to explore the function and mechanism of 5'tiRNA‑Gln‑TTG‑001. Cell viability, apoptosis rates, and levels of factors associated with inflammation (IL‑1β, IL‑6 and IL‑18), myocardial injury (creatine kinase MB and high‑sensitivity cardiac troponin) and myocardial dysfunction (N‑terminal pro‑B‑type natriuretic peptide) were quantified to assess the degree of cardiomyocyte inflammatory injury. RNA fluorescence <i>in situ</i> hybridization (RNA‑FISH), cell transfection, dual‑luciferase reporter assays and functional experiments, including gain‑of‑function and loss‑of‑function assays and rescue experiments, were carried out to further explore the underlying mechanisms. The results revealed that 5'tiRNA‑Gln‑TTG‑001 was upregulated in acute myocarditis and positively correlated with high‑sensitivity cardiac troponin T and T2 ratio. <i>In vitro</i> experiments demonstrated that 5'tiRNA‑Gln‑TTG‑001 aggravated cardiomyocyte inflammatory injury. RNA‑FISH revealed co‑localization of 5'tiRNA‑Gln‑TTG‑001 and chloride intracellular channel 4 (CLIC4) in the nucleus and cytoplasm. Gain‑of‑function and loss‑of‑function experiments revealed that 5'tiRNA‑Gln‑TTG‑001 promoted CLIC4 expression. Dual‑luciferase reporter assays indicated that 5'tiRNA‑Gln‑TTG‑001 activated CLIC4 by binding to its 3'untranslated region. Furthermore, downregulation of CLIC4 rescued cardiomyocyte inflammatory injury aggravated by 5'tiRNA‑Gln‑TTG‑001. Meanwhile, the knockdown of 5'tiRNA‑Gln‑TTG‑001 reduced cardiomyocyte inflammatory injury and the effect was reversed by the upregulation of CLIC4. Overall, the present study demonstrated that 5'tiRNA‑Gln‑TTG‑001 may aggravate cardiomyocyte inflammatory injury via CLIC4 upregulation. Moreover, 5'tiRNA‑Gln‑TTG‑001 could offer a promising option for the diagnosis of myocarditis and serve as a potential therapeutic target.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708203","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":"Pan‑cancer analysis of the carcinogenic role of WSB2 in human tumors.","authors":"Yingzi Deng, Yifei Li, Ruobing Li, Xiaohui Guo, Yan Liu, Shuqing Wang, Juan Zhang, Mi Li, Lina Zhao, Haifeng Cai, Yunfeng Zhang, Fen Hu","doi":"10.3892/mmr.2025.13625","DOIUrl":"10.3892/mmr.2025.13625","url":null,"abstract":"<p><p>WD repeat and SOCS box containing 2 (WSB2) is an E3 ubiquitin ligase that might be involved in regulating protein stability, thus performing important roles in the development of different types of cancer. However, the biological significance of WSB2 in pan‑cancer is unclear. Pan‑cancer analysis with the online platforms UALCAN and TIMER2.0. revealed that the expression levels of WSB2 were increased in various types of tumors, including breast invasive carcinoma, uterine corpus endometrial carcinoma, liver hepatocellular carcinoma and were decreased in other types such as colon adenocarcinoma, kidney chromophobe and rectum adenocarcinoma, compared with that in their corresponding normal tissues. In addition, pan‑cancer analysis using The Human Protein Atlas database indicated that WSB2 expression levels vary across different cancer types. Reverse transcription‑quantitative PCR (RT‑qPCR) revealed that WSB2 expression varied in 11 different cell lines. Promoter activity analysis indicates that specificity protein 1 carries out a key role in regulating WSB2 expression by binding to its promoter region. UALCAN and Kaplan‑Meier analysis were used to assess the pathological stage and prognostic value of WSB2 in pan‑cancer. Finally, overexpression of WSB2 promoted the proliferation and migration of MCF‑7 and MDA‑MB‑231 cells. Western blotting revealed that WSB2 increased the levels of vimentin, Snail and ERK1/2, and inhibited the expression of p53 and E‑cadherin in MDA‑MB‑231 and MCF‑7 cells. Transcriptome sequencing analysis identified 118 differentially expressed genes associated with WSB2 overexpression, which were mainly enriched in the 'p53 signaling pathway'. Furthermore, the expression of NUPR1 (encoding nuclear protein 1, transcriptional regulator), LDLRAD4 (encoding low density lipoprotein receptor class A domain containing 4) and MDM2 (encoding mouse double min 2) were verified by RT‑qPCR. Overall, the present study contributes to the understanding of the carcinogenic role of WSB2 in different types of cancer.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708206","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}