The FASEB Journal最新文献

{"title":"Characterizing Elephant MDM2's Role in p53 Regulation","authors":"Emma Palefsky,&nbsp;Himani K. Patel,&nbsp;Trey A. Doss,&nbsp;Emilye C. Eischeid,&nbsp;Paul Lee,&nbsp;MacLaren A. Durkee,&nbsp;William H. Yang,&nbsp;Avery M. Duncan,&nbsp;Darshti Patel,&nbsp;Anmol P. Patel,&nbsp;Wei-Hsiung Yang,&nbsp;Jong-Hyuk Lee","doi":"10.1096/fj.202502511R","DOIUrl":"https://doi.org/10.1096/fj.202502511R","url":null,"abstract":"<div>\u0000 \u0000 <p>Peto's paradox, which describes the absence of a strong correlation between cancer risk, body size, and lifespan among species, raises intriguing questions about natural cancer resistance mechanisms. Elephants have evolved unique adaptations that reduce cancer susceptibility despite their large body size and long lifespan. Central to this phenomenon is p53, a key tumor suppressor regulated by MDM2. Our research investigates the structural and functional differences between elephantine MDM2 and its human counterpart. Utilizing human cellular models, we demonstrate that elephantine MDM2 variants enhance p53's activity, leading to increased p53 occupancy on its response elements, and modulate p53-mediated transcription in a stress-dependent manner. These findings shed light on the molecular basis of cancer resistance in elephants and provide a foundation for developing innovative cancer therapies targeting MDM2-p53 interactions.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TET2 Deficiency Exacerbates Podocyte Injury and Mitophagy Disorder in Diabetic Nephropathy by Regulating M5C Methylation of Bcas3","authors":"Xiao-han Ma,&nbsp;Zi-yun Hu,&nbsp;Yu-kai Wang,&nbsp;Yu Ma,&nbsp;Guang-peng Liu,&nbsp;Xue-qi Liu","doi":"10.1096/fj.202500946R","DOIUrl":"https://doi.org/10.1096/fj.202500946R","url":null,"abstract":"<div>\u0000 \u0000 <p>Recent evidence highlights the critical role of 5-methylcytidine (m5C) as an epigenetic modification in the pathogenesis of various diseases. However, its regulatory mechanisms in diabetic nephropathy (DN) remain poorly understood. In this study, we observed a marked increase in m5C levels in the kidneys of type 2 diabetic (db/db) mice and in high glucose (HG)-stimulated podocytes, which was linked to reduced expression of the m5C demethylase ten-eleven translocation 2 (TET2). Moreover, renal biopsy samples from patients with DN exhibited decreased TET2 expression, correlating with impaired renal function. Gain-of-function assays revealed that TET2 overexpression in HG-induced podocytes enhanced mitophagy and ameliorated podocyte injury both in vitro and in vivo. Therapeutically, systemic delivery of AAV-TET2 in db/db mice reduced albuminuria, improved renal histopathology, and restored mitophagy. Mechanistically, TET2 regulated mitophagy by modulating the m5C methylation of Breast Carcinoma Amplified Sequence 3 (Bcas3). Furthermore, Bcas3 overexpression promoted mitophagy and attenuated podocyte damage under HG conditions. In conclusion, TET2-mediated m5C modification contributes to podocyte injury in DN, and targeting m5C via TET2 presents a promising therapeutic strategy for DN.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Creatine Supplementation Enhances Fat Graft Survival by Mitochondrial Protection and Revascularization Promotion","authors":"Min-Chen Zhang,&nbsp;Yuan-Zheng Zhu,&nbsp;Shu Wu,&nbsp;Heng-Yu Wu,&nbsp;Su-jun Pei,&nbsp;Xing-hong Zeng,&nbsp;Ying Peng,&nbsp;Ying Ding,&nbsp;Yang-Yan Yi","doi":"10.1096/fj.202501473R","DOIUrl":"10.1096/fj.202501473R","url":null,"abstract":"<div>\u0000 \u0000 <p>Autologous fat grafting is compromised by post-grafting ischemic necrosis and volumetric resorption, clinical challenges stemming from inadequate vascularization and metabolic stress. Here, we identify oral creatine supplementation as a translatable metabolic therapy to enhance fat graft survival. Through adipose organoids and a murine grafting model, we demonstrate that creatine stabilizes mitochondrial membrane potential (ΔΨm), reduces reactive oxygen species (ROS), and redirects energy production toward non-mitochondrial ATP synthesis, collectively promoting adipocyte survival and revascularization. Mechanistically, creatine activates a phosphocreatine-kinase shuttle to sustain ATP pools independently of oxidative phosphorylation, while concurrently mitigating electron transport chain-derived oxidative damage. The therapeutic equivalence of systemic and localized delivery routes, combined with creatine's FDA-approved safety profile, positions this intervention as a clinically viable strategy to improve fat grafting outcomes.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Transcriptomic and Proteomic Analysis of Omentin-1 Effects on Primary Anterior Pituitary Cells From Different Pig Breeds: An In Vitro Study","authors":"Natalia Respekta-Długosz,&nbsp;Karolina Pich,&nbsp;Edyta Rytelewska,&nbsp;Bianka Świderska,&nbsp;Agata Malinowska,&nbsp;Jakub Chatys,&nbsp;Christelle Ramé,&nbsp;Joëlle Dupont,&nbsp;Tadeusz Kamiński,&nbsp;Nina Smolińska,&nbsp;Agnieszka Rak","doi":"10.1096/fj.202502202R","DOIUrl":"10.1096/fj.202502202R","url":null,"abstract":"<div>\u0000 \u0000 <p>Omentin-1 (OMNT1) is a metabolically active adipokine implicated in endocrine regulation; however, its role in the anterior pituitary (AP) remains unknown. We hypothesized that OMNT1 modulates the endocrine function of AP cells through gene- and protein-level mechanisms, with effects depending on the animal's metabolic background. To investigate this hypothesis, AP cells isolated from two pig breeds with distinct metabolic profiles, Large White (LW; normal weight) and Meishan (MS; genetically obese), were treated with OMNT1. Transcriptomic and proteomic analyses were performed alongside assessments of hormone expression and secretion. Transcriptomic profiling revealed 13 310 and 13 272 expressed genes in LW and MS pigs, respectively. Differentially expressed gene (DEG) analysis revealed 655 DEGs in LW pigs and 420 in MS pigs. Integrated transcriptomic and proteomic analyses revealed that OMNT1 modulates pathways involved in cellular signaling, cytoskeleton dynamics, responses to stimuli, intracellular protein transport, and post-translational modifications. We further examined the mRNA expression and secretion of tropic hormones (GH, PRL, TSH, ACTH, LH, and FSH) and selected adipokines (adiponectin, leptin, chemerin, apelin, visfatin, resistin, and vaspin), along with their specific receptors. OMNT1 increased LH secretion and decreased FSH levels in a breed-dependent manner. Additionally, in MS pigs, OMNT1 reduced adiponectin and increased leptin secretion. These findings highlight the role of OMNT1 as a key modulator of pituitary endocrine activity, integrating metabolic signals through breed-specific molecular responses at the transcriptional, proteomic, and functional levels.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CXCR7 Facilitates the Migration and Proliferation of UCMSCs via β-Catenin/TCF4/MDM2 Signal Regulating Notch1 Ubiquitination to Ameliorate Pulmonary Fibrosis in ARDS","authors":"Yan Cao,&nbsp;Zhirong Qian,&nbsp;Yuwei Yang,&nbsp;Jiahui Jin,&nbsp;David Y. B. Deng,&nbsp;Shuning Zhang,&nbsp;Lixin Xie,&nbsp;Kun Xiao","doi":"10.1096/fj.202500609RR","DOIUrl":"10.1096/fj.202500609RR","url":null,"abstract":"<div>\u0000 \u0000 <p>Umbilical cord mesenchymal stem cells (UCMSCs) hold therapeutic potential for acute respiratory distress syndrome (ARDS), but the role of atypical CXC chemokine receptor 7 (CXCR7) in their homing and reparative effects remains unclear. Using a lipopolysaccharide (LPS)-induced ARDS mouse model, we demonstrated that CXCR7 overexpression enhances UCMSC proliferation, migration, and lung repair. Mechanistically, CXCR7 activates the Wnt/β-catenin pathway to upregulate murine double minute (MDM2) transcription, which subsequently ubiquitinates and degrades Notch1, revealing a novel Wnt-Notch crosstalk. These findings highlight CXCR7 as a therapeutic target for ARDS and provide insights into UCMSC-based regenerative strategies.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Alleviates Retina Angiogenesis by Targeting Fibronectin and the VEGF Pathway","authors":"Fang Chen,&nbsp;Xi Yang,&nbsp;Yiwei Yin,&nbsp;Zhishang Meng,&nbsp;Ze Wu,&nbsp;Dan Liu,&nbsp;Chengkun Wu,&nbsp;Jing Luo,&nbsp;Wenyi Wu","doi":"10.1096/fj.202500814RR","DOIUrl":"10.1096/fj.202500814RR","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetic retinopathy (DR) and retinopathy of prematurity (ROP) continue to be significant causes of vision impairment despite the well-established role of vascular endothelial growth factor (VEGF) in pathological angiogenesis. We still need to deeply understand retinal angiogenesis's molecular mechanisms and identify potential alternate therapeutic targets. We used RNA sequencing (RNA-seq) and found fibronectin (<i>FN1</i>), an extracellular matrix protein, was significantly upregulated during retinal angiogenesis in the oxygen-induced retinopathy (OIR) model. Employing a deep learning model (BioNet) to identify potential <i>FN1</i> inhibitors among FDA-approved drugs, we discovered that melatonin effectively reduced <i>FN1</i> expression and inhibited VEGF-induced angiogenesis by decreasing VEGFR2 phosphorylation. In vivo, melatonin administration significantly reduced preretinal tufts in the OIR model while suppressing <i>FN1</i> expression and VEGFR2 activation. This study highlights the power of computer-driven drug discovery, with BioNet successfully identifying melatonin as a potential therapeutic agent for retinal angiogenesis. The ability of melatonin to inhibit both <i>FN1</i> and VEGF signaling highlights the potential of integrating advanced computational methods with rigorous experimental validation to uncover novel therapies for complex diseases.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNFSF4 Promotes Bone Erosion in Rheumatoid Arthritis by Enhancing the Inflammatory Response of Synovial Macrophages","authors":"Xiaoyu Cai,&nbsp;Yao Yao","doi":"10.1096/fj.202501883RR","DOIUrl":"10.1096/fj.202501883RR","url":null,"abstract":"<div>\u0000 \u0000 <p>Tumor necrosis factor superfamily member 4 (TNFSF4), also known as OX40L, is implicated in autoimmune diseases, but its role in rheumatoid arthritis (RA) remains poorly understood. This study reveals that TNFSF4 expression is elevated in RA synovial tissue and correlates with disease activity markers. Using a collagen-induced arthritis (CIA) mouse model, we demonstrate that TNFSF4 exacerbates synovial inflammation and promotes bone erosion by skewing macrophage polarization toward the pro-inflammatory M1 phenotype. TNFSF4 knockout reduces M1 macrophages, increases M2 macrophages, and attenuates cytokine-driven inflammation and osteoclast activity. Importantly, TNFSF4 does not directly modulate macrophage polarization but requires CD4⁺ T cell involvement. These findings uncover a novel mechanism by which TNFSF4 contributes to RA pathogenesis and highlight its potential as a therapeutic target for modulating immune responses and preventing joint damage in RA.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145202038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circRNA_0101125 Promotes Proliferation, Migration, and Invasion of Esophageal Squamous Cell Carcinoma via miR-143-3p/ZNF148 Axis","authors":"Hao Chen,&nbsp;Songtao Xue,&nbsp;Shiqiang Cao,&nbsp;Jiarong Zhang,&nbsp;Yuanpu Wei,&nbsp;Chun Chen,&nbsp;Guobing Xu","doi":"10.1096/fj.202500257R","DOIUrl":"10.1096/fj.202500257R","url":null,"abstract":"<p>Esophageal squamous cell carcinoma (ESCC) is a highly invasive and metastatic malignancy. Circular RNAs (circRNAs), including hsa_circRNA_0101125, have been implicated in regulating cancer metastasis. But its potential roles in ESCC remain underexplored, particularly in relation to miR-143-3p. This study aimed to investigate the role of hsa_circRNA_0101125/miR-143-3p in the occurrence and development of ESCC. KYSE150 and ECA109 cells were used as in vitro models to evaluate the biological effects of hsa_circRNA_0101125. The interaction between ZNF148 and miR-143-3p was confirmed by dual-luciferase assay. To assess the functional role of this pathway, cells were transfected with sh-hsa_circRNA_0101125 vectors and/or miR-143-3p inhibitors, followed by assays for cell viability (CCK-8), migration (wound healing assay), and invasion (Transwell assay). Transcriptions and expressions of hsa_circRNA_0101125, miR-143-3p, and ZNF148 were measured by RT-qPCR and western blot. Results showed that hsa_circRNA_0101125 was localized in the cytoplasm and negatively regulated miR-143-3p, which targeted ZNF148. Inhibition of hsa_circRNA_0101125 significantly reduced cell viability, migration, and invasion, downregulated ZNF148 and Vimentin, and upregulated miR-143-3p and E-cadherin expressions. In contrast, downregulating miR-143-3p abolished these effects. Therefore, hsa_circRNA_0101125 promotes the proliferation, migration, and invasion of ESCC cells by inhibiting the expression of miR-143-3p.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycolytic Metabolite 3-Phosphoglycerate Induced by Inflammation Inhibits Chondrocyte Survival","authors":"Yan Zhao,&nbsp;Wei-Jin Gao,&nbsp;Yan Xue,&nbsp;Jia-Nan Zhang,&nbsp;Zhi-Yong Li,&nbsp;Qian-Ming Chen,&nbsp;Meng-Jie Wu","doi":"10.1096/fj.202501650R","DOIUrl":"10.1096/fj.202501650R","url":null,"abstract":"<div>\u0000 \u0000 <p>The reduction of chondrocytes is an important pathological manifestation in the cartilage degeneration, and the abnormal metabolism of chondrocytes triggered by inflammation is the key reason for the inhibition of chondrocyte survival. The enhancement of glycolysis is an important feature of chondrocyte metabolism in inflammatory environments, but the effects of metabolic enzymes and metabolites on chondrocyte survival in this process are still unclear. In this study, we used transcriptomics to analyze the expression of glycolytic metabolic enzymes in condylar chondrocytes under inflammatory environments (IL-1β, 10 ng/mL) and identified phosphoglycerate kinase 1 (PGK1), the metabolic enzyme with the most significant increase in glycolysis, as well as improving the condylar chondrocytes survival and cartilage degeneration after inhibiting PGK1 activity. Subsequently, in metabolomics studies, we found that 3-phosphoglycerate (3-PGA), a direct metabolite of PGK1, increased significantly, and it was the most significantly increased among all detectable and labeled carbohydrate-related metabolites. Furthermore, condylar chondrocytes showed obvious survival inhibition in the presence of increased 3-PGA. Finally, we screened out the downstream molecule CXCL10 through transcriptomics-based joint analysis and computer algorithm selection. In summary, this study used transcriptomics and metabolomics, combined with cellular function and histological examination, to identify and validate that the metabolite of PGK1, 3-PGA, accumulates in the condylar chondrocytes in inflammatory environment, leading to significant inhibition of their survival. It specifically elucidates the molecular mechanism of enhanced glycolysis by which inflammation leads to inhibition of condylar chondrocytes survival, providing theoretical basis for understanding condylar cartilage degeneration from a metabolic perspective.</p>\u0000 </div>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"STC1-Based Activation of NF-κB Signaling Pathway Induces Epthithelial–Mesenchymal Transition Thus Promotes Progression and Temozolomide Resistance of Glioblastoma","authors":"Jia Wang,&nbsp;Beichen Zhang,&nbsp;Haoyu Zhou,&nbsp;Bin Liu,&nbsp;Xiaobin Bai,&nbsp;Wei Wu,&nbsp;Ruichun Li,&nbsp;Wanfu Xie","doi":"10.1096/fj.202500095R","DOIUrl":"10.1096/fj.202500095R","url":null,"abstract":"<p>Acquired resistance to chemotherapy, especially to temozolomide (TMZ), is a major challenge correlated with the treatment failure of glioblastoma (GBM). Stanniocalcin-1 (STC1) is a glycoprotein hormone involved in multiple biological processes in cancer cells. However, the function and underlying mechanism of STC1 in GBM still remain unclear. To this end, exploring the potential functional role and mechanism of STC1 inducing TMZ resistance becomes an urgent need for individual individualized strategies for GBM. The GSE151680 dataset was obtained from the GEO database; thus, bioinformatic analysis was performed by using R software (version 4.2.0) to screen the differentially expressed genes correlated to TMZ resistance in GBM. Cox regression and nonnegative matrix factorization (NMF) analysis were conducted to establish a prognostic model. Additionally, immunohistochemistry (IHC) staining, qRT-PCR, and western blot were used to investigate the expression of STC1 in GBM tissues and non-tumor controls. Mechanically, loss-of-function and gain-of-function assays were performed to validate the biological functions of STC1 on the malignant biological characters and TMZ resistance of GBM cells. Besides, the enrichment analysis was performed to investigate the downstream pathway of STC1. In this study, STC1 was selected as the gene candidate correlated to TMZ resistance according to the results of Cox regression and NMF analysis. Additionally, increased expression of STC1 could be observed in GBM and was significantly correlated to poor prognosis in GBM. Besides, multiple malignant characters including proliferation, migration, invasion, tumorigenesis, and TMZ resistance of GBM could be markedly reduced by exogenous downregulation of STC1; contrarily, overexpression of STC1 promoted the malignant behaviors and drug resistance of GBM cells. Moreover, GO, KEGG, and GSEA analysis revealed that STC1 induced epithelial-mesenchymal transition (EMT) via activation of NF-κB signaling. Furthermore, the treatment of TNF-α (an activator of the NF-κB pathway) partially reversed the inhibitory effect of sh-STC1 on the proliferation and metastasis in GBM cells. In conclusion, STC1 induced EMT thus enhances the malignancies and drug resistance of GBM cells by activating the NF-κB pathway, providing new evidence for clinical drug development in GBM.</p>","PeriodicalId":50455,"journal":{"name":"The FASEB Journal","volume":"39 19","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}