Experimental cell research最新文献

{"title":"The BET degrader BETd-246 demonstrated significant anti-tumor efficacy in T-cell acute lymphoblastic leukemia by inhibiting TRAT1","authors":"Haixia Ge ,&nbsp;Huike Bai ,&nbsp;Juanjuan Yu ,&nbsp;Jia Cheng ,&nbsp;Zhongqin Jin ,&nbsp;Jian Pan ,&nbsp;Xue Li ,&nbsp;Chunxia Shi ,&nbsp;Yang Yang ,&nbsp;Shaoyan Hu ,&nbsp;Yanfang Tao","doi":"10.1016/j.yexcr.2025.114791","DOIUrl":"10.1016/j.yexcr.2025.114791","url":null,"abstract":"<div><div>T cell acute lymphoblastic leukemia (T-ALL) is a rare lymphoblastic leukemia characterized by T lymphocyte heterogeneity and diverse genetic abnormalities, accounting for approximately 15 % of childhood leukemias. BETd-246 serves as a tethering agent that links BETi-211 to thalidomide for the development of BET degraders. This compound has demonstrated superior efficacy in tumor treatment compared with traditional BET inhibitors. However, the anti-tumor effects and molecular mechanisms underlying the action of BETd-246 in T-ALL remain poorly understood. The aim of our study was to investigate the anti-tumor effects of BETd-246 and provide new insights into treatment strategies for T-ALL. In human T-ALL cell lines, BETd-246 induced degradation of BET proteins, particularly BRD4, at nanomolar concentrations. It effectively inhibited cell growth, disrupted the cell cycle, and promoted apoptosis in T-ALL cells in a concentration-dependent manner. The effects of BETd-246 were more pronounced than those of JQ1. <em>In vivo</em> experiments revealed that treatment with BETd-246 reduced proliferation and invasion of T-ALL cells and extended survival time in mouse models. RNA sequencing analysis indicated significant downregulation of T-cell receptor (TCR)-associated transmembrane adaptor 1 (TRAT1) expression in T-ALL cells treated with BETd-246. Knocking down TRAT1 resulted in increased growth inhibition and enhanced apoptosis within these cells. These findings suggest that TRAT1 plays a crucial role in mediating the effects of BETd-246 in T-ALL. Overall, our results indicate that BETd-246 is a promising therapeutic agent for treating this aggressive form of leukemia.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114791"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to ‘Simvastatin inhibits the development of radioresistant esophageal cancer cells by increasing the radiosensitivity and reversing EMT process via the PTEN-PI3K/AKT pathway’ [Exp Cell Res. 2018 Jan 15;362(2):362–369]","authors":"Yingying Jin,&nbsp;Kun Xu,&nbsp;Qingjuan Chen,&nbsp;Baofeng Wang,&nbsp;Jiyuan Pan,&nbsp;Shan Huang,&nbsp;Yang Wei,&nbsp;Hongbing Ma","doi":"10.1016/j.yexcr.2025.114792","DOIUrl":"10.1016/j.yexcr.2025.114792","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114792"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal protein restriction promotes cardiac disorders by disrupting heart developmental morphophysiology in young male offspring rats","authors":"Lucas Sobrinho Lemos ,&nbsp;Matheus Naia Fioretto ,&nbsp;Isabelle Tenori Ribeiro ,&nbsp;Luísa Annibal Barata ,&nbsp;Flávia Alessandra Maciel ,&nbsp;Felipe Leonardo Fagundes ,&nbsp;Renato Mattos ,&nbsp;Luiz Marcos Frediani Portela ,&nbsp;João Miguel Barboza ,&nbsp;Beatriz Souza de Oliveira ,&nbsp;Keila Emílio de Almeida ,&nbsp;Sérgio Alexandre Alcantara dos Santos ,&nbsp;Clélia Akiko Hiruma Lima ,&nbsp;José Ricardo de Arruda Miranda ,&nbsp;Elena Zambrano ,&nbsp;Luis Antonio Justulin","doi":"10.1016/j.yexcr.2025.114795","DOIUrl":"10.1016/j.yexcr.2025.114795","url":null,"abstract":"<div><div>In recent years, cardiovascular diseases have been one of the leading causes of death worldwide. Epidemiological and experimental studies have linked adverse intrauterine conditions with an susceptibility to cardiovascular and metabolic diseases in subsequent generations, a concept related to the Developmental Origins of Health and Disease (DOHaD). Here, we evaluated the maternal protein restriction (MPR), and its harmful effects on the cardiac morphophysiology of offspring in early life. During gestation and lactation, the pregnant rats were divided into two groups: Control (CTR), which received a normoprotein diet (17 % protein), and Gestational and Lactational Low-Protein (GLLP), which received a hypoprotein diet (6 % protein). At postnatal day 21, the offspring were euthanized. There was a decrease in serum levels of IGF1, an increase in testosterone, and a decrease in several phenotypic parameters in the heart, such as the size of cardiomyocytes and their nuclei, collagen, reticular and elastic fibers, and mast cells in the GLLP group. We observed that MPR led to electrical disorders in the heart (bradycardia), in addition to impacting angiogenic proteins (high Aquaporin1 and PECAM-1), and proteins associated with the antioxidant system (low Peroxiredoxin 4 and high GSTpi expressions) in the GLLP group. These adverse effects early in life increase the risk of pathophysiological remodeling of the heart, with the potential for hypertension, hypertrophy, and cardiovascular disease later in life.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114795"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epitranscriptomic analysis reveals features of NAD-capped RNAs upon supplementation of nicotinamide mononucleotide in human","authors":"Shuwen Ge ,&nbsp;Yandong Liu ,&nbsp;Dean Li ,&nbsp;Guojing Han ,&nbsp;Kongyan Niu ,&nbsp;Hujun Ju ,&nbsp;Hao Zhou ,&nbsp;Rui Liu ,&nbsp;Zhengjiang Zhu ,&nbsp;Nan Liu ,&nbsp;Lefeng Qu","doi":"10.1016/j.yexcr.2025.114780","DOIUrl":"10.1016/j.yexcr.2025.114780","url":null,"abstract":"<div><div>Nicotinamide mononucleotide (NMN), a precursory metabolite of NAD, has been demonstrated to boost cellular NAD level that is coupled with various age-related beneficial effects in animal models. NAD-capped RNA (NAD-RNA) represents a critical but poorly studied modification at the epitranscriptomic level. Here we examine the impact of NMN supplementation on NAD-RNA in human peripheral blood mononuclear cells (PBMCs). We demonstrated that NMN supplementation increases NAD turnover coupled with a reduction in NAD-capped RNAs in both human and dog, revealing blood-derived NAD-RNAs as potential biomarkers sensitized to NMN exposure.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114780"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNF216P1 functions as an oncogenic gene through modulating miR-195-5p/ATG4B axis in hepatocellular carcinoma","authors":"Kai Li ,&nbsp;Yaping Bai ,&nbsp;Jingtong Wang ,&nbsp;Li Ren ,&nbsp;Anqi Mo ,&nbsp;Haijun Liu ,&nbsp;Wenjun Pei","doi":"10.1016/j.yexcr.2025.114797","DOIUrl":"10.1016/j.yexcr.2025.114797","url":null,"abstract":"<div><div>Recent studies have highlighted the critical roles of long non-coding RNAs (lncRNAs) in tumorigenesis and progression. Here, we report that the lncRNA RNF216P1 is significantly upregulated in hepatocellular carcinoma (HCC) and contributes to tumor growth. To elucidate its underlying mechanisms, we first analyzed the transcriptional levels of RNF216P1 and its targets, miR-195-5p and autophagy related 4B cysteine peptidase (ATG4B), in HCC tissues using The Cancer Genome Atlas dataset, followed by validation with RT-qPCR. ATG4B protein levels were assessed by Western blotting. Functional assays—including xenograft models, CCK-8 viability tests, wound-healing assays, and Transwell migration assays—were performed to evaluate the role of RNF216P1 in HCC progression. Furthermore, the interactions between RNF216P1 and miR-195-5p, as well as between miR-195-5p and ATG4B, were confirmed by fluorescence in situ hybridization (FISH), RNA immunoprecipitation assays, and dual-luciferase reporter assays. Collectively, our findings demonstrate that RNF216P1 promotes malignant progression in HCC cells by acting as a competing endogenous RNA for miR-195-5p, thereby upregulating ATG4B and enhancing autophagy. This study identifies a novel ceRNA axis—RNF216P1/miR-195-5p/ATG4B—that plays a pivotal role in HCC development and may represent a potential therapeutic target.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114797"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NOTCH signaling orchestrates the inflammatory-fibrotic continuum of macrophages in renal allograft rejection","authors":"Yanxu Chen ,&nbsp;Qiang Zhang ,&nbsp;Wenyu Xie ,&nbsp;Pengfei Gao ,&nbsp;Zhaowei Hu ,&nbsp;Shenghui Wu ,&nbsp;Zirong Bi ,&nbsp;Huanxi Zhang ,&nbsp;Yifang Gao ,&nbsp;Changxi Wang ,&nbsp;Longshan Liu","doi":"10.1016/j.yexcr.2025.114711","DOIUrl":"10.1016/j.yexcr.2025.114711","url":null,"abstract":"<div><h3>Background</h3><div>Chronic rejection is a major cause of long-term kidney allograft failure, characterized by persistent inflammation and progressive fibrosis. Macrophages are central mediators of this process, but their phenotypic heterogeneity and regulatory mechanisms in chronic rejection remain incompletely understood.</div></div><div><h3>Methods</h3><div>We performed single-cell transcriptomic analysis on renal allograft biopsies from patients with different types of rejection and on a time-course rat model of chronic rejection. Macrophage subsets were identified through transcriptional profiling and Pseudotime trajectory analysis. Ligand–receptor analysis defined upstream intercellular communication, while in vitro assays using THP-1 macrophages evaluated responses to Jagged1 stimulation under polarizing conditions.</div></div><div><h3>Results</h3><div>A distinct TGFB⁺CD86⁺ macrophage subset exhibiting both pro-inflammatory and pro-fibrotic features was identified. This population, enriched in mixed rejection, occupied an intermediate position along the inferred macrophage trajectory and displayed dual ontogeny. It received Jagged1–NOTCH2 signals from mesenchymal-transitioned tubular epithelial cells and inflammatory inputs from infiltrating T cells. In vitro, co-stimulation with soluble Jagged1 under M1-polarizing conditions induced a similar hybrid phenotype. In the rat model, a phenotypically comparable subset, provisionally termed M2b, appeared early post-transplantation and was later replaced by M2a macrophages as fibrosis progressed. Ligand–receptor analysis confirmed conserved Jagged1–NOTCH2 signaling regulatory axis in vivo.</div></div><div><h3>Conclusion</h3><div>In summary, we identify a transitional TGFB⁺CD86⁺ macrophage population governed by JAG1–NOTCH2 signaling, bridging immune activation and fibrotic remodeling. Modulating this pathway may offer a therapeutic approach to reshape macrophage differentiation and mitigate chronic rejection.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114711"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deficiency of vitamin D-binding protein exacerbates liver fibrosis by disrupting iron homeostasis via the activation of YAP signaling","authors":"Qing Zheng ,&nbsp;Qingquan Tan ,&nbsp;Dan Wang ,&nbsp;Yanling Ma ,&nbsp;Yanni Zhou ,&nbsp;Yonghua Chen ,&nbsp;Dan Long ,&nbsp;Jiayin Yang ,&nbsp;Li Feng","doi":"10.1016/j.yexcr.2025.114767","DOIUrl":"10.1016/j.yexcr.2025.114767","url":null,"abstract":"<div><div>Liver fibrosis is a chronic progressive disease that can advance to cirrhosis or hepatocellular carcinoma if untreated. While liver transplantation remains the only curative option for end-stage fibrosis, the development of alternative therapies is urgently needed. In this study, we investigated the role of vitamin D-binding protein (VDBP) in hepatic fibrosis using clinical samples and a CCl₄-induced mouse model. We observed significant downregulation of VDBP in fibrotic human and murine livers, suggesting that VDBP may serve as a potential biomarker for disease progression. VDBP knockout (VDBP-KO) mice exhibited exacerbated fibrosis, iron overload, and ferroptosis activation, accompanied by dysregulation of the Hippo-YAP pathway. In vitro, VDBP overexpression reversed these effects, while in vivo treatment with the YAP inhibitor verteporfin attenuated fibrosis, normalized iron homeostasis, and suppressed ferroptosis in VDBP-KO mice. Our findings demonstrate that VDBP plays a pivotal role in maintaining iron balance, inhibiting YAP signaling, and preventing ferroptosis during fibrogenesis. Elucidating the molecular mechanisms of VDBP and its downstream pathways may provide novel therapeutic targets for liver fibrosis. This could significantly improve the clinical management of hepatic fibrosis and offer new hope for patients suffering from this debilitating disease.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114767"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SOCS1 orchestrates ferroptotic renal injury via GPX4 ubiquitination in hyperuricemia","authors":"Renzhong Zhang,&nbsp;Xu Fu,&nbsp;Xiaoli Zhao,&nbsp;Ke Wang","doi":"10.1016/j.yexcr.2025.114774","DOIUrl":"10.1016/j.yexcr.2025.114774","url":null,"abstract":"<div><div>Hyperuricemia (HUA)-induced renal injury involves elusive molecular mechanisms. This study uncovers suppressor of cytokine signaling 1 (SOCS1) as a pivotal mediator of hyperuricemic nephropathy through ferroptosis regulation. In a murine HUA model, we observed significantly elevated serum uric acid, impaired renal function, heightened inflammation, and activated ferroptosis. <em>In vitro</em> studies using uric acid-treated renal tubular cells demonstrated that SOCS1 deficiency alleviated ferroptotic cell death, reduced inflammatory responses, and preserved mitochondrial integrity. Mechanistically, SOCS1 directly interacts with glutathione peroxidase 4 (GPX4) to promote its ubiquitin-dependent proteasomal degradation, as validated by co-immunoprecipitation and protein stability assays. Crucially, pharmacological induction of ferroptosis abolished the protective effects of SOCS1 knockdown, while GPX4 inhibition counteracted its anti-ferroptotic function. <em>In vivo</em> delivery of renal-targeted SOCS1 shRNA <em>via</em> AAV9 vectors attenuated hyperuricemic nephropathy, ameliorating histological damage and suppressing both ferroptosis and inflammation. Our findings establish a pathogenic axis wherein SOCS1 drives hyperuricemic renal injury by facilitating GPX4 ubiquitination and subsequent ferroptosis activation, highlighting this pathway as a promising therapeutic target.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114774"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145174398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human trophoblast stem cell-differentiated syncytiotrophoblasts as a model for hypoxia-enhanced secretion of the anti-angiogenic factor sFLT1","authors":"Tadashi Sasagawa,&nbsp;Masabumi Shibuya","doi":"10.1016/j.yexcr.2025.114773","DOIUrl":"10.1016/j.yexcr.2025.114773","url":null,"abstract":"<div><div>Preeclampsia (PE) is a major disease in the field of obstetrics. Onset and progression of PE are associated with abnormally high serum levels of soluble fms-like tyrosine kinase-1 (sFLT1), an anti-angiogenic factor primarily secreted by syncytiotrophoblasts (STBs) present in the placenta. Although a cell-based assay using primary human trophoblasts has been developed to identify compounds that inhibit sFLT1 secretion, routine application of this assay is limited owing to the complexity of isolating these cells from the placenta and their inability to be passaged. Recently, human trophoblast stem cell (hTSC) lines that can differentiate into STBs and extravillous trophoblasts have been established. Their high proliferative ability allows for obtaining sufficient STBs for drug screening. In the present study, we investigated whether hTSC-differentiated STBs (dSTBs) exhibit enhanced secretion of sFLT1 under hypoxic conditions, similar to primary trophoblasts. Hypoxic stimulation significantly increased sFLT1 secretion by the dSTBs. This response was markedly inhibited by small interfering RNAs targeting the hypoxia-inducible factor (HIF)-2α and HIF-1β, as well as by the HIF-2α inhibitor, belzutifan. These findings suggest that the dSTBs described above are a practical and scalable alternative to primary trophoblasts for drug screening in PE treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114773"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145174428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ALYREF stabilizes CREPT mRNA to accelerate the development of nasopharyngeal carcinoma through dependence on m5C modification","authors":"Danni Xu ,&nbsp;Yu Fu ,&nbsp;Huamao Sun ,&nbsp;Yanda Lu ,&nbsp;Bo Shen ,&nbsp;Xinbao Hao","doi":"10.1016/j.yexcr.2025.114747","DOIUrl":"10.1016/j.yexcr.2025.114747","url":null,"abstract":"<div><h3>Background</h3><div>Nasopharyngeal carcinoma (NPC) is a kind of tumor disease with high malignant degree. CREPT expression was elevated abnormally in multi-cancers. However, the role and regulatory mechanism of CREPT in NPC remains unknown.</div></div><div><h3>Methods</h3><div>NPC clinical samples, NPC cells, and nude mice served as experimental objects. The levels of molecules were detected using RT-qPCR,Western blot, IF and IHC experiments. Malignant activities of NPC cells were evaluated using CCK-8, EdU and clone formation, flow cytometry and TUNEL. Kaplan-Meier and Pearson correlation analysis were employed to analysis of the relationships between CREPT expression and prognosis/ALYREF expression in NPC patients. The interaction between ALYREF and CREPT was validated using RIP, RNA pull-down and dual luciferase experiment.</div></div><div><h3>Results</h3><div>Upregulation of CREPT and ALYREF expression was observed in NPC samples including the tissues of NPC patients and cells. CREPT knockdown reduced NPC cell viability, proliferation and enhanced NPC cell apoptosis and suppressed tumor growth through deactivating Wnt/β-catenin pathway, but the results of ALYREF overexpression had the inverse results of CREPT knockdown. Furthermore, the combination of CREPT knockdown and ALYREF overexpression compromised ALYREF overexpression-mediated the influences on NPC cells, tumor growth and motivating Wnt/β-catenin pathway. Furthermore, ALYREF interacted with CREPT mRNA and ALYREF promoted the stability of CREPT mRNA in m5C-dependent manner.</div></div><div><h3>Conclusion</h3><div>ALYREF stabilized CREPT mRNA through interacting with m5C-labeled CREPT mRNA to elevate CREPT expression, thus activating Wnt/β-catenin pathway and facilitating NPC progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114747"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}