Experimental cell research最新文献

{"title":"LncRNA HANR promotes the aerobic glycolysis in prostate cancer by stabilizing TPI1","authors":"Ziye Wang,&nbsp;Xiaoguang Li,&nbsp;Zhengdao Liu,&nbsp;Yang Du,&nbsp;Tao Wu","doi":"10.1016/j.yexcr.2025.114744","DOIUrl":"10.1016/j.yexcr.2025.114744","url":null,"abstract":"<div><div>Prostate cancer (PCa) is a type of malignancy that originates in the prostate gland, often characterized by uncontrolled cell growth and potential metastasis. Long non-coding RNAs (lncRNAs) play crucial regulatory roles in the progression of prostate cancer, potentially facilitating tumor growth and metastasis via mechanisms that involve the enhancement of aerobic glycolysis. This study aimed to investigate the functional role of lncRNA HANR in prostate cancer progression. Bioinformatics analysis and experimental validation revealed a significant up-regalation of HANR in prostate cancer tissues, in comparison to adjacent normal tissues. Functional studies demonstrated that silencing HANR inhibited prostate cancer cells proliferation, migration, invasion, and glycolysis. While HANR overexpression promoted prostate cancer cells proliferation, invasion, and glycolysis. Mechanistically, HANR interacts with triosephosphate isomerase 1 (TPI1), a key glycolytic enzyme, to promote glycolysis and tumor growth. Silencing HANR or TPI1 reduced prostate tumor growth both <em>in vitro</em> and <em>in vivo</em>. In conclusion, our findings suggest that the HANR-TPI1 axis plays a crucial role in the progression of prostate cancer and may represent a novel biomarker and therapeutic target for aggressive prostate cancer, given its role in enhancing aerobic glycolysis and facilitating tumorigenesis in prostate cancer cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114744"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023197","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":"JPH203 alleviates renal fibrosis via inhibition of serine-related mTORC1 pathway in TGF-β1-induced fibroblasts and UUO mice","authors":"Changwan Cui ,&nbsp;Mengqi Hong ,&nbsp;Hainan Zhao ,&nbsp;Lei Wang ,&nbsp;Ying Yang ,&nbsp;Jingyu Wang ,&nbsp;Li Sun","doi":"10.1016/j.yexcr.2025.114732","DOIUrl":"10.1016/j.yexcr.2025.114732","url":null,"abstract":"<div><div>Renal fibrosis is the common pathological outcome of chronic kidney disease (CKD) progressing into end-stage renal disease. The excessive proliferation of fibroblasts plays an important role in the CKD progression. Nutrients such as amino acids and their transportation are essential for cell proliferation. In this study, TGF-β1-induced fibroblasts and UUO mouse models were used. The target gene solute carrier family 7 member 5 (SLC7A5) was screened to be highly expressed and localized in the renal fibroblasts of CKD mice. In vivo experiments showed that SLC7A5 promoted the activation of mammalian target of rapamycin complex 1 (mTORC1) signaling pathway, enhanced serine synthesis and maintained oxidative stress balance in fibroblasts. SLC7A5 increased the expression of transcription factor activating transcription factor 4 (ATF4), promoted the transcription of serine de-novo synthesis enzyme PHGDH, and increased the synthesis of glutathione, a byproduct of serine synthesis pathway. JPH203, a specific inhibitor of SLC7A5, effectively reversed the above phenomena, inhibited mTORC1 signaling activation, and reduced the proliferation of fibroblasts. The efficacy of JPH203 was further verified by in vivo experiments. JPH203 had a similar effect to the inhibitory adenovirus AV-shSLC7A5 in the UUO mouse model. Compared with the UUO group, the activation of mTORC1 pathway in the JPH203 treatment group was inhibited, and the expressions of α-SMA and vimentin in fibroblasts were decreased. The fibrotic state of renal tissues was effectively relieved. In addition, the levels of serum creatinine, blood urea nitrogen and pelvic urinary protein were significantly decreased compared with the UUO group. In conclusion, our study demonstrated that JPH203 can alleviate renal fibrosis via inhibition of serine-related mTORC1 pathway in fibroblasts in UUO mice. These results may provide a theoretical foundation for the pathogenesis of renal fibrosis and a novel therapeutic strategy for CKD.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114732"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014159","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":"HMGB1 contributes to pancreatic fibrosis by regulating TLR4-mediated autophagy and the NLRP3 inflammasome pathway in chronic pancreatitis","authors":"Caixia Li ,&nbsp;Lihua Cui ,&nbsp;Yanjie Zuo ,&nbsp;Jianhong Pan ,&nbsp;Xiao Li ,&nbsp;Xinsheng Xu ,&nbsp;Lanqiu Zhang ,&nbsp;Yuzhen Zhuo ,&nbsp;Guowang Yao ,&nbsp;Zhenyu Wang ,&nbsp;Shukun Zhang","doi":"10.1016/j.yexcr.2025.114745","DOIUrl":"10.1016/j.yexcr.2025.114745","url":null,"abstract":"<div><div>The characteristic pathological change in chronic pancreatitis (CP) is pancreatic fibrosis. In the early stages of CP development, injured acinar cells induce the infiltration of inflammatory cells, followed by pancreatic stellate cell (PSC) activation. Activated PSC induce the deposition of extracellular matrix (ECM) and promote the development of pancreatic fibrosis. High-mobility group Box 1 (HMGB1) is a damage-associated molecular pattern (DAMP) molecule. Although HMGB1 is implicated in several types of fibrotic diseases, its functional role and mechanism in pancreatic fibrosis in CP remain unknown. In this study, a dibutyltin dichloride (DBTC)-induced rat CP model was constructed in vivo. The results revealed that HMGB1 translocates from the nucleus of acinar cells to the cytoplasm and is subsequently released into the extracellular space, thereby promoting the progression of pancreatic fibrosis in CP. PSC was isolated and exposed to varying concentrations of HMGB1 in vitro. Resatorvid and <em>si-TLR4</em> were applied to verify that the functions of HMGB1 were realized by combining with TLR4. 3-MA, <em>si</em>-<em>Atg5</em> and MCC950 were used to determine the effect of HMGB1 on PSC activation through the regulation of autophagy and the NLRP3 inflammasome. These results indicated that exogenous administration of HMGB1 induces PSC activation and ECM deposition through its receptor TLR4. Mechanistically, the HMGB1/TLR4 axis promoted PSC activation by promoting autophagy–NLRP3 inflammasome activation. Our study highlights the profibrotic role of HMGB1 and provides a novel therapeutic target for the treatment of CP.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114745"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145014192","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":"SIRT1 rescues autophagic flux via PI3K/AKT/mTOR inactivation to suppress DOX-induced senescence in MCF-7 cells","authors":"Ge Wu ,&nbsp;Wei Yao ,&nbsp;Lin Cheng ,&nbsp;Xiaoping Wang ,&nbsp;Tongsheng Chen","doi":"10.1016/j.yexcr.2025.114754","DOIUrl":"10.1016/j.yexcr.2025.114754","url":null,"abstract":"<div><div>Sirtuin 1 (SIRT1), a deacetylase, has been extensively studied for its roles in regulating autophagy, aging, cellular metabolism and tumorigenesis. In this study, we investigated how SIRT1 modulates doxorubicin (DOX)-induced senescence in MCF-7 cells, a breast cancer cell line. SIRT1 significantly reduced the DOX-induced elevation of senescence-associated proteins p53, p21, and SA-β-Gal activity, revealing that SIRT1 inhibited DOX-induced senescence. Notably, SIRT1 increased the DOX-induced upregulation of p62 accumulation and reversed the DOX-induced decrease in the LC3II/LC3I ratio, revealing that SIRT1 reversed the DOX-induced blockage of autophagic flux. The autophagy inhibitor chloroquine (CQ) partially abolished the anti-aging effects of SIRT1, indicating that autophagy mediated the anti-aging effects of SIRT1. Additionally, SIRT1 suppressed the DOX-induced activation of the phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, thereby facilitating autophagy. The PI3K inhibitor LY294002 enhanced the anti-aging effect of SIRT1 which, however, was reversed by the AKT activator SC-79. In conclusion, our study reveals that SIRT1 counteracts DOX-induced senescence in MCF-7 cells by inactivating PI3K/AKT/mTOR pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114754"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080151","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":"A floating endometrial organoid model recapitulates epithelial-stromal cell interactions in vitro","authors":"Adriana Bajetto ,&nbsp;Alessandra Pattarozzi ,&nbsp;Alessandro Corsaro ,&nbsp;Beatrice Tremonti ,&nbsp;Monica Gatti ,&nbsp;Valerio Pisaturo ,&nbsp;Luisa Campagnolo ,&nbsp;Denise Colia ,&nbsp;Elena Pastine ,&nbsp;Alessandra Alteri ,&nbsp;Mauro Costa ,&nbsp;Stefano Thellung ,&nbsp;Federica Barbieri ,&nbsp;Tullio Florio","doi":"10.1016/j.yexcr.2025.114749","DOIUrl":"10.1016/j.yexcr.2025.114749","url":null,"abstract":"<div><div>Organoids are 3D structures in which stem, progenitor and differentiated cells spontaneously assemble into structures resembling the original tissue. Endometrial organoids, developed from tissue fragments, are genetically stable and responsive to hormone stimulation acquiring a hallow lumen, secretory activity and apico-basal polarity. However, they show some limitations in mimicking the midluteal endometrium since they lack endothelial, immune, and stromal cells, thus providing limited information about epithelial-stromal interactions. We developed a 3D-model to generate endometrial organoids in floating Matrigel™ droplets using standard medium. Floating organoids form gland-like structures constituted by epithelial cells organized around a central lumen, and contain stromal cells grown in close contact, either outside or inside the organoid structure. Similarly to conventional endometrial organoids, floating organoids retain the expression of endometrial and decidual genes, assessed by qRT-PCR for a panel of fifteen genes, although with a pattern of expression resembling, in most cases, what observed in hormonally differentiated organoids. In conclusion, we describe a simple and rapid model to generate 3D endometrial organoids, ensuring the persistence of epithelial-stromal cell interaction, which fosters the development of differentiated organoids, thereby enabling the study of the reciprocal modulation between epithelium and stroma.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114749"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032868","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":"The effect and mechanism of CXCL9 overexpressed umbilical cord mesenchymal stem cells on liver fibrosis in vivo and in vitro","authors":"Yang Li ,&nbsp;Xueqian Zhang ,&nbsp;Guiyu Liu ,&nbsp;Tianci Tang ,&nbsp;Xueshuai Ye ,&nbsp;Jianhui Cai","doi":"10.1016/j.yexcr.2025.114750","DOIUrl":"10.1016/j.yexcr.2025.114750","url":null,"abstract":"<div><h3>Background</h3><div>Umbilical cord mesenchymal stem cells (UC-MSCs) transplantation has emerged as a promising therapeutic approach of liver fibrosis. However, UC-MSCs have limited anti-fibrotic ability for various reasons. In this study, we aimed to investigate whether the overexpression of CXCL9 in UC-MSCs (CXCL9-UC-MSC) could have synergistic anti-fibrotic effects and explore the possible mechanism.</div></div><div><h3>Methods</h3><div>We established the rat models of liver fibrosis and administered CXCL9-UC-MSC cells via tail vein injection for therapy. We assessed the improvement in liver lesion and liver function across different treatment groups, while further investigating the expression of various proteins within the TGF-β1/Smad3 signaling pathway. Additionally, we monitored the expression levels of α-SMA, Collagen-III and Collagen-I. In vitro studies were conducted using activated LX-2 cells to validate the cellular pathways and assess inhibition of activation.</div></div><div><h3>Results</h3><div>After cell therapy, pathological staining and liver function indicated that the area of liver fibrosis in the rats was reduced, the hepatocellular necrosis was alleviated, and liver function damage was improved. Notably, these improvements were more significant in the CXCL9-UC-MSC group. Furthermore, the expression levels of α-SMA, Collagen-III, Collagen-I, TGF-β1 and pSmad3 in the liver and LX-2 cells were significantly decreased after the CXCL9 intervention. Additionally, the abilities of proliferation, viability and invasiveness of LX-2 cells were also significantly inhibited with the intervention of CXCL9.</div></div><div><h3>Conclusion</h3><div>The overexpression of CXCL9 in UC-MSCs inhibited the activation of the TGF-β1/Smad3 signaling pathway, and reduced the expressions of α-SMA, Collagen-III and Collagen-I in liver and LX-2 cells, thereby exerting a more significant anti-fibrotic effect.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114750"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039509","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":"PRDX3 promotes nasopharyngeal carcinoma tumor growth by regulating PINK1/Parkin pathway-dependent lipid peroxidation and mitochondrial dysfunction","authors":"Hualong Qiang ,&nbsp;Wei Wang ,&nbsp;Xiaodong Zhan ,&nbsp;Shiyin Ma","doi":"10.1016/j.yexcr.2025.114731","DOIUrl":"10.1016/j.yexcr.2025.114731","url":null,"abstract":"<div><h3>Background</h3><div>Nasopharyngeal carcinoma (NPC) is a challenging malignancy characterized by aggressive progression and limited therapeutic efficacy. Emerging evidence implicates peroxiredoxin 3 (PRDX3), a mitochondrial peroxidase, as a critical regulator of redox homeostasis and mitochondrial integrity. Given its role in modulating cell death through mitochondrial quality control, we investigated the therapeutic potential of targeting PRDX3 in NPC.</div></div><div><h3>Methods</h3><div>PRDX3 expression patterns were assessed in clinical NPC specimens using immunohistochemical and immunoblotting. Functional studies employed siRNA-mediated PRDX3 knockdown followed by cellular assays: CCK-8 proliferation, clonogenic survival, and mitochondrial parameter quantification (reactive oxygen species flux using DCFH-DA/C11-BODIPY, ATP biosynthesis, membrane polarization, and mtDNA integrity). Molecular interplay between PRDX3 and PTEN-induced kinase 1 (PINK1) was elucidated through co-immunoprecipitation and immunofluorescence analysis. In vivo therapeutic efficacy was validated using a xenograft model to evaluate tumor growth modulation.</div></div><div><h3>Results</h3><div>Clinical specimens revealed significant PRDX3 overexpression in NPC compared to non-malignant controls. PRDX3 knockdown substantially attenuated malignant behavior and induced mitochondrial dysfunction in NPC cells. Mechanistically, PRDX3 interacted with PINK1 to stabilize Parkin-mediated mitophagic flux. PRDX3 safeguarded against apoptosis by sustaining PINK1/Parkin-dependent mitophagy clearance of damaged mitochondria. In vivo validation confirmed that PRDX3 knockdown suppressed tumor growth.</div></div><div><h3>Conclusion</h3><div>PRDX3 acts as an upstream activator of the PINK1/Parkin signaling cascade, regulating lipid peroxidation-mediated mitochondrial dysfunction, mitophagy, survival and apoptosis of NPC cell.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 1","pages":"Article 114731"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006020","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":"Inhibition of HMGN2 SUMOylation ameliorates atherosclerosis by activating PAX5 expression to induce macrophage M2 polarization","authors":"Xiangkui Wang ,&nbsp;Peipei Wu ,&nbsp;Yadi Shen ,&nbsp;Shiwei Xu ,&nbsp;Qi Wan ,&nbsp;Yongfei Yang","doi":"10.1016/j.yexcr.2025.114709","DOIUrl":"10.1016/j.yexcr.2025.114709","url":null,"abstract":"<div><h3>Background</h3><div>As a core pathological process of cardiovascular disease, atherosclerosis (AS) progression is closely linked to macrophage polarization, yet the mechanisms by which post-translational modifications regulate inflammatory responses in AS remain unclear.</div></div><div><h3>Methods</h3><div>Using oxidized low-density lipoprotein (ox-LDL)-induced RAW264.7 foam macrophages and high-fat diet-fed (apolipoprotein E knockout) ApoE^−/− mice, we assessed HMGN2 SUMOylation's role in macrophage M2 polarization. Cell proliferation/migration were analyzed via EdU/Transwell assays; macrophage polarization phenotypes were examined by immunofluorescence. Inflammatory cytokines and NF-κB pathway were quantified using ELISA/Western blot. Aortic plaque formation and lipid deposition were evaluated through HE staining and Oil Red O lipid visualization.</div></div><div><h3>Results</h3><div>In cellular experiments, research demonstrated that HMGN2 enhances interaction with the transcription factor PAX5 through SUMOylation, thereby inhibiting PAX5 activity and driving macrophage polarization toward the pro-inflammatory M1 phenotype. Furthermore, PIAS1 knockdown significantly reduced HMGN2 SUMOylation levels. This disruption suppressed the binding between PAX5 and HMGN2 and reduced inflammatory factor release. Animal experiments revealed that targeted PIAS1 knockdown markedly reduced aortic plaque area, improved lipid metabolic disorders, and modulated inflammatory cytokines by inhibiting NF-κB signaling pathway.</div></div><div><h3>Conclusion</h3><div>The present study systematically reveals the molecular mechanism by which HMGN2 SUMOylation regulates macrophage polarization and inflammatory response through the \"PAX5-NF-κB\" signaling axis, which may become a new target for the treatment of atherosclerosis by targeting epigenetic modification.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 2","pages":"Article 114709"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144887092","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 “Secreted AGR2 promotes invasion of colorectal cancer cells via Wnt11-mediated non-canonical Wnt signaling” [Exp. Cell. Res. 364(2) (2018)198–207]","authors":"Shaobo Tian ,&nbsp;Jia Hu ,&nbsp;Kaixiong Tao ,&nbsp;Jian Wang ,&nbsp;Yanan Chu ,&nbsp;Jing Li ,&nbsp;Zhibo Liu ,&nbsp;Xueliang Ding ,&nbsp;Luming Xu ,&nbsp;Qilin Li ,&nbsp;Ming Cai ,&nbsp;Jinbo Gao ,&nbsp;Xiaoming Shuai ,&nbsp;Guobin Wang ,&nbsp;Lin Wang ,&nbsp;Zheng Wang","doi":"10.1016/j.yexcr.2025.114655","DOIUrl":"10.1016/j.yexcr.2025.114655","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 2","pages":"Article 114655"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505274","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 ‘Analysis of the in vitro response of the Sapajus cay (Primates: Platyrrhini) genome to exposure to the radiomimetic bleomycin’ [Exp. Cell Res. 450 (2025) 114689]","authors":"Mariela Nieves ,&nbsp;Romina Celeste Páez ,&nbsp;Esteban Orlando Ferreras ,&nbsp;Melina Noelia Ortuño Orgaz ,&nbsp;Nancy Beatriz Andrioli","doi":"10.1016/j.yexcr.2025.114698","DOIUrl":"10.1016/j.yexcr.2025.114698","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"451 2","pages":"Article 114698"},"PeriodicalIF":3.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855004","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}