JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"Correction to “The Uyghur Population and Genetic Susceptibility to Type 2 Diabetes: Potential Role for Variants in CAPN10, APM1 and FUT6 Genes”","authors":"","doi":"10.1111/jcmm.70638","DOIUrl":"https://doi.org/10.1111/jcmm.70638","url":null,"abstract":"<p>Zhao F, Mamatyusupu D, Wang Y, Fang H, Wang H, Gao Q, Dong H, Ge S, Yu X, Zhang J, Wu L, Song M, Wang W. The Uyghur Population and Genetic Susceptibility to Type 2 Diabetes: Potential Role for Variants in CAPN10, APM1 and FUT6 genes. <i>J Cell Mol Med</i>. 2016;20(11):2138-2147.</p><p>In the Acknowledgements section, the Australian National Health and Medical Research Council (NHMRC-APP1112767) and the Edith Cowan University Strategic Research Fund (SRF-2015) should be removed.</p><p>The Acknowledgement statement reads:</p><p>This study was supported by research grants from the National Natural Science Foundation of China (81573215, 81273170, 31460285 and 81370083), National 12th Five-Year Major Projects of China (2012BAI37B03), Australian National Health and Medical Research Council and National Natural Science Foundation of China (NHMRC-APP1112767-NSFC 81561128020), Edith Cowan University Strategic Research Fund (SRF-2015), Natural Science Foundation of Xinjiang Uyghur Autonomous Region (2013211A016), and Natural Science Foundation of Capital Medical University, Beijing, China (2014ZR16). Manshu Song was supported by the Importation and Development of High-Calibre Talents Project of Beijing Municipal Institutions (CIT&amp;TCD201404185). The authors thank the Uyghur volunteers and community leaders for their supports and participation. We appreciate the English editing by Eric Adua, School of Medical Sciences and Health, Edith Cowan University, Australia.</p><p>The Acknowledgement statement should read:</p><p>This study was supported by research grants from the National Natural Science Foundation of China (81573215, 81273170, 31460285, 81370083 and 81561128020), National 12th Five-Year Major Projects of China (2012BAI37B03), Natural Science Foundation of Xinjiang Uyghur Autonomous Region (2013211A016) and Natural Science Foundation of Capital Medical University, Beijing, China (2014ZR16). Manshu Song was supported by the Importation and Development of High-Calibre Talents Project of Beijing Municipal Institutions (CIT&amp;TCD201404185). The authors thank the Uyghur volunteers and community leaders for their supports and participation. We appreciate the English editing by Eric Adua, School of Medical Sciences and Health, Edith Cowan University, Australia.</p><p>We apologize for this error.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Omaveloxolone Suppresses Cell Growth and Causes Cell Cycle Arrest by Downregulating CDC20 Expression in Glioblastoma Cells Both In Vitro and In Vivo","authors":"Kuan-Ting Lee,&nbsp;Yi-Chiang Hsu,&nbsp;Ann-Shung Lieu,&nbsp;Chih-Lung Lin,&nbsp;Tai-Hsin Tsai","doi":"10.1111/jcmm.70607","DOIUrl":"https://doi.org/10.1111/jcmm.70607","url":null,"abstract":"<p>Omaveloxolone is a synthetic oleanane triterpene with considerable antitumor activity. It induces human glioblastoma (GBM) cell death in vitro and in vivo, but the underlying mechanism remains to be determined. In this study, GBM cell lines (GBM8401 and U-87 MG cells) were exposed to different concentrations of omaveloxolone (0, 600, 800 and 1000 nM). A cell viability assay was conducted using the PrestoBlue Cell Viability Reagent. Three-dimensional microscopy revealed changes in cell morphology. Cell cycle, apoptosis and mitochondrial membrane potential were tested using flow cytometry. The expression levels of cell cycle-related proteins and genes were determined through Western blotting and next-generation sequencing, respectively. The results indicated that omaveloxolone had significant selective cytotoxicity against human GBM cells and suppressed the migration and invasion of these cancer cells. It also caused cell cycle arrest through the downregulation of cell cycle-related genes, including cell division cycle 20 homologue (<i>CDC20</i>), as revealed by next-generation sequencing. In a xenograft tumour model, omaveloxolone decreased tumour volume and CDC20 expression. Taken together, these findings suggest that omaveloxolone is a potential drug candidate for GBM treatment by promoting GBM cell death through the downregulation of CDC20 expression.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70607","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathological Glucose Levels Enhance Entry Factor Expression and Hepatic SARS-CoV-2 Infection","authors":"Guocheng Rao,&nbsp;Xiongbo Sang,&nbsp;Xinyue Zhu,&nbsp;Sailan Zou,&nbsp;Yanyan Zhang,&nbsp;Wei Cheng,&nbsp;Yan Tian,&nbsp;Xianghui Fu","doi":"10.1111/jcmm.70581","DOIUrl":"https://doi.org/10.1111/jcmm.70581","url":null,"abstract":"<p>Accumulating clinical evidence suggests an intricate relationship between severe COVID-19 and preexisting metabolic complications, which share some metabolic dysregulations, including hyperglycaemia, hyperinsulinaemia and hyperlipidaemia. However, the potential role of these metabolic risk factors in SARS-CoV-2 infection and entry factor expression remains unknown. Here we report the implication of hyperglycaemia in SARS-CoV-2 infection and therapy. Hyperglycaemia, instead of hyperinsulinaemia and hyperlipidaemia, can significantly induce the expression of SARS-CoV-2 entry factors (<i>Ace2</i>, <i>Tmprss2</i>, <i>Tmprss4</i>, <i>Furin</i> and <i>Nrp1</i>) in liver cells, but not in lung and pancreatic cells, which is attenuated by mTOR inhibition. Correspondingly, pathological glucose levels promote SARS-CoV-2 entry into cultured hepatocytes in pseudovirus cell systems. Conversely, representative glucose-lowering drugs (metformin, dapagliflozin, sitagliptin and exenatide) are able to diminish the enhancement of entry factor expression and SARS-CoV-2 infection in cultured hepatocytes under pathological glucose conditions. Intriguingly, SARS-CoV-2 entry factors are increased in the livers of nonalcoholic fatty liver disease and diabetes patients. These results define hyperglycaemia as a key susceptibility factor for hepatic SARS-CoV-2 infection, and provide insights into the clinical application of glucose-lowering therapies in COVID-19 patients under comorbid hyperglycaemia conditions.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70581","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Signature of Breast Cancer Defines Therapeutic Interventions and Indicates Early Drug Resistance","authors":"Angeliki Margoni,&nbsp;Kostas A. Papavassiliou,&nbsp;Athanasios G. Papavassiliou","doi":"10.1111/jcmm.70635","DOIUrl":"https://doi.org/10.1111/jcmm.70635","url":null,"abstract":"<p>Breast cancer (BC) is the most prevalent cancer in women and ranks first in diagnosed cancers worldwide, thanks to effective screening strategies. However, morbidity and mortality rates remain high among aggressive subtypes, forcing oncologists to adopt the philosophy of precision oncology in clinical practice. Immunohistochemical analysis of the tumour establishes diagnosis and stratifies BC into four types, according to a globally recognised classification. Tumour cells present a wide diversity in morphological, histological and molecular characteristics, indicating the heterogeneous nature of BC that reflects on different proliferation rates, risks of relapse and metastasis. The differentiation in prognosis and response to treatment underscores the vital need for targeted therapy, specific for each tumour's genetic status, that enhances therapeutic effectiveness. The aim of the present article is to designate the potential of using a novel molecular modality as a diagnostic tool that enlightens oncologists during their therapeutic decisions and raises awareness of therapeutic failure. Next-generation sequencing (NGS) detects a wide gamut of biomarkers and gene mutations in biopsy samples, revealing the precise genetic profile and implicating a personalised therapy. Incorporation of molecular testing in the diagnostic algorithm promises amelioration of therapeutic outcomes, prevention of recurrence and reduction of BC-related mortality.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70635","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Inflammatory Mediators in Pericardial Fluids of Patients With Coronary Artery Diseases and Their Association With Plasma Biomarkers","authors":"Reşat Dikme,&nbsp;Mehmet Salih Aydın,&nbsp;Ebru Temiz,&nbsp;İsmail Koyuncu,&nbsp;Mesut Işık","doi":"10.1111/jcmm.70625","DOIUrl":"https://doi.org/10.1111/jcmm.70625","url":null,"abstract":"<p>The aim of this study was to determine the gene expression and protein levels of interleukin-33 (IL-33), fetuin A and cytokeratin 18 (CK-18) in the pericardial fluid (PF) and plasma of patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting (CABG). The CAD patients (mean age: 73.4 years) were enrolled. The IL-33, fetuin A, and CK-18 protein levels in pericardial fluid (PF) and plasma of patients with CAD were measured by ELISA, while IL-33 and Fetuin A gene expressions were analysed via quantitative reverse transcription-PCR (qRT-PCR). The IL-33 protein level in PF was significantly higher than plasma (PF: 57.09 ng/L; Plasma: 50.15 ng/L; <i>p</i> &lt; 0.05). Similarly, the fetuin A protein levels were significantly elevated in PF compared to plasma (PF: 1060.53 mg/L; Plasma: 725.85 mg/L; <i>p</i> &lt; 0.05). However, gene expression levels (ΔCt values) for IL-33 and fetuin A were significantly higher in plasma than in PF (<i>p</i> &lt; 0.05). The CK-18 protein levels were comparable between plasma and PF (<i>p</i> &gt; 0.05). Strong positive correlations were observed between CK-18 and IL-33 (<i>r</i> = 0.127, <i>p</i> &lt; 0.001) and between CK-18 and fetuin A (<i>r</i> = 0.096, <i>p</i> &lt; 0.001) in PF. The IL-33, fetuin A, and CK-18 levels in PF are predicted to have the potential to be used as a source of biomarkers for CAD. Although the collection of PF samples requires an invasive procedure, the proximity of PF to the heart tissue makes it a valuable source for understanding cardiac pathophysiology. These findings highlight the potential diagnostic and therapeutic utility of PF biomarkers in patients with CAD.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70625","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Efficacy of Hellebrigenin Against Nasopharyngeal Carcinoma Cells: The Molecular and Bioinformatic Analysis","authors":"Hsin-Yu Ho,&nbsp;Mu-Kuan Chen,&nbsp;Yun-Jung Tsai,&nbsp;Chia-Chieh Lin,&nbsp;Yu-Sheng Lo,&nbsp;Yi-Ching Chuang,&nbsp;Ming-Ju Hsieh","doi":"10.1111/jcmm.70624","DOIUrl":"https://doi.org/10.1111/jcmm.70624","url":null,"abstract":"<p>Nasopharyngeal carcinoma (NPC) is a unique cancer type originating from the nasopharynx. To investigate novel strategies for improving prognosis and reducing the adverse effects of current treatments, this study examined the efficacy of hellebrigenin. Hellebrigenin demonstrated selective cytotoxicity against NPC-BM and NPC-039 cell lines without harming normal nasopharyngeal cells. Treatment with hellebrigenin resulted in G2/M cell cycle arrest in both NPC cell lines. The apoptotic phenomena induced by hellebrigenin included chromatin condensation, increased apoptotic cells and altered mitochondrial membrane potential. Proteomics analysis and the bioinformatic data identified coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2) as a candidate oncogene in NPC. Moreover, the combination of CHCHD2 siRNA, CHCHD2 plasmid and hellebrigenin pointed out that CHCHD2 could be a critical mediator of hellebrigenin-induced apoptosis. The combined treatment of hellebrigenin with mitogen-activated protein kinase inhibitors revealed the involvement of the extracellular signal–regulated kinases and c-Jun N-terminal kinases pathways in hellebrigenin-induced apoptosis in NPC cells. In vivo studies demonstrated that hellebrigenin suppressed the tumour volume without affecting body weight, accompanied by the downregulation of Ki67 and CHCHD2 expression. In conclusion, this study provides evidence that hellebrigenin induces NPC apoptosis through regulating CHCHD2 both in vitro and in vivo.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70624","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OVOL1 Promotes Proliferation and Metastasis of Non-Small Cell Lung Cancer by Regulating APOE-Mediated Cholesterol Metabolism","authors":"Shoujie Feng,&nbsp;Li Zhang,&nbsp;Teng Sun,&nbsp;Lei Xu,&nbsp;Xiaoyu Quan,&nbsp;Guoqing Zhao,&nbsp;Hao Zhang","doi":"10.1111/jcmm.70634","DOIUrl":"https://doi.org/10.1111/jcmm.70634","url":null,"abstract":"<p>Non-small cell lung cancer (NSCLC) is a highly lethal malignant tumour characterised by its resistance to treatment, often due to metabolic reprogramming. Despite this, the underlying mechanisms by which aberrant cholesterol metabolism influences the development and progression of NSCLC remain unclear. In our study, we observed that OVOL1 is significantly upregulated in NSCLC and is correlated with a poor prognosis. Furthermore, our functional assays revealed that OVOL1 enhances the proliferation and metastasis of NSCLC cells both in vitro and in vivo. Mechanistically, OVOL1 was found to modulate cholesterol reprogramming and increase the expression of APOE, thereby intensifying cholesterol metabolism and facilitating cell migration and invasion. In conclusion, our findings suggest that OVOL1 acts as an oncogene in NSCLC, promoting tumour growth and metastasis through the enhancement of cholesterol metabolism. This underscores the potential of OVOL1 as a therapeutic target for the treatment of NSCLC.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70634","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-486-5p Inhibits eNOS and Angiogenesis in Cultured Endothelial Cells by Targeting MAML3","authors":"Adrianna Douvris,&nbsp;Ali Maadelat,&nbsp;Christopher J. Porter,&nbsp;Dylan Burger,&nbsp;Kevin D. Burns","doi":"10.1111/jcmm.70589","DOIUrl":"https://doi.org/10.1111/jcmm.70589","url":null,"abstract":"<p>Kidney ischemia–reperfusion (I/R) is associated with endothelial injury. Administration of miRNA (miR)-486-5p protects against rat kidney I/R injury, with localisation to capillary endothelial cells, although it inhibits I/R-induced endothelial nitric oxide synthase (eNOS) protein expression. Here, we studied the effect of miR-486-5p on eNOS and endothelial cell function and determined its mRNA targets. Human umbilical vein endothelial cells (HUVECs) were transfected with the miR-486-5p mimic and assayed for proliferation, migration and network formation. Biotinylated miR-486-5p was transfected for pulldown of bound mRNA, followed by RNA sequencing. miR-486-5p markedly decreased eNOS mRNA and protein in HUVECs (<i>p</i> &lt; 0.001) and decreased eNOS protein in human pulmonary microvascular endothelial cells (<i>p</i> &lt; 0.05), although eNOS was not a direct target of miR-486-5p. miR-486-5p inhibited angiogenesis, which was rescued with eNOS plasmid transfection. RNA sequencing of biotinylated miR-486-5p pulldown RNA revealed highly significant enrichment in predicted targets FOXO1, FOXP1, TNFSF4, MAML3 and CELSR3, and in the non-predicted target SPCS2. RT-qPCR validated these transcripts as inhibited by miR-486-5p. While silencing of FOXO1 had no impact on eNOS protein, MAML3 silencing inhibited eNOS levels. miR-486-5p inhibits angiogenesis in endothelial cells via eNOS down-regulation, which involves selective targeting of MAML3. These data support a novel pathway regulating endothelial cell function.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 11","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70589","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of METTL3 on MDM2 Promotes Podocytes Injury During Diabetic Kidney Disease","authors":"Han Wu,&nbsp;Ziyang Yu,&nbsp;Yitian Yang,&nbsp;Zhuoting Han,&nbsp;Qingjun Pan,&nbsp;Ying Chen,&nbsp;Hongyuan Yu,&nbsp;Siman Shen,&nbsp;Li Xu","doi":"10.1111/jcmm.70627","DOIUrl":"https://doi.org/10.1111/jcmm.70627","url":null,"abstract":"<p>N6-Methyladenosine (m6A) methylation plays a role in various pathological processes, including renal fibrosis and aging. Our previous studies have highlighted abnormal expression of the methyltransferase enzyme, methyltransferase like 3 (METTL3), in aging kidney tissues. This study aims to elucidate the regulatory mechanisms of METTL3 in diabetic kidney disease (DKD) by establishing a conditional METTL3 knockout model. We observed elevated m6A levels in the kidneys of type I diabetic mice and in cultured mouse podocytes exposed to advanced glycation end products (AGEs). These increases were attributed to enhanced METTL3 expression. Significantly, podocyte-specific METTL3 knockdown mitigated injury in streptozotocin (STZ)-induced diabetic mice, evidenced by reduced urine albuminuria and renal pathology. We discovered that METTL3 induced abnormal m6A modification of murine double minute 2 (MDM2), which triggered its degradation in an IGF2BP2 (insulin-like growth factor 2 mRNA-binding protein 2)-dependent manner. This modification led to increased MDM2 expression, activating the Notch signalling pathway and inducing podocyte cell cycle arrest under diabetic conditions, which further released inflammatory factors and caused podocyte dedifferentiation. Our findings suggest that targeting m6A modification via METTL3 could be an effective strategy for treating DKD.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 10","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70627","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144140834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sohlh1 Modulates the Stemness and Differentiation of Glioma Stem-Like Cells by Inactivation of Wnt/β-Catenin Signalling Pathway via SFRP1","authors":"Sujuan Zhi,&nbsp;YanRu Chen,&nbsp;Yunling Xiao,&nbsp;Lanlan Liu,&nbsp;Xiaoning Feng,&nbsp;Xuyue Liu,&nbsp;Ying Shen,&nbsp;RuiHong Zhang,&nbsp;Jing Hao","doi":"10.1111/jcmm.70599","DOIUrl":"https://doi.org/10.1111/jcmm.70599","url":null,"abstract":"<p>Glioma stem-like cells (GSLCs) are tumour initiating cells that drive tumorigenesis and progression through self-renewal and various differentiation potencies. Therefore, the identification of genes required for GSLC stemness and differentiation is vital for the development of novel targeted therapies. Sohlh1 belongs to the superfamily of bhlh transcription factors and serves as a tumour suppressor in glioma. The role of Sohlh1 in GSLCs remains unknown. Here, we demonstrated that Sohlh1 functioned through the SFRP1/Wnt/β-catenin signalling pathway and led to the consequent suppression of GSLC stemness and the promotion of GSLC differentiation in vitro and in vivo. Moreover, Sohlh1 could directly bind to the promoter of SFRP1 and promote its transcriptional activity. SFRP1 mediated the effects of Sohlh1 on GSLC stemness and differentiation. Clinically, we observed a significant inverse correlation between Sohlh1 and Nestin expression levels, and a positive correlation between Sohlh1 and SFRP1 expression in glioma tissues. Collectively, our findings suggest an important role of the Sohlh1/SFRP1/Wnt/β-catenin pathway in regulating GSLC stemness and differentiation, suggesting potential therapeutic targets for glioma.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 10","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70599","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}