Experimental cell research最新文献

{"title":"Pan-carcinoma data driven analysis reveals platelet-activating factor receptor (PTAFR) involvement in immunosuppressive tumor microenvironment signaling and clinical prognosis","authors":"Barbara Dalmaso ,&nbsp;Ildefonso Alves da Silva-Junior ,&nbsp;Sonia Jancar ,&nbsp;Laura Steenpass ,&nbsp;Carolina Beltrame Del Debbio ,&nbsp;Claudia Pommerenke","doi":"10.1016/j.yexcr.2025.114643","DOIUrl":"10.1016/j.yexcr.2025.114643","url":null,"abstract":"<div><div>Solid tumor carcinogenesis is driven by complex interactions within the tumor microenvironment (TME), which influence tumor initiation, progression, and response to treatment. The phospholipid platelet-activating factor (PAF) has been described to affect TME and growth; however, evidence so far has been limited to experimental <em>in vitro</em> and <em>in vivo</em> models. This study investigates the role of PAF receptor (PTAFR) across various carcinomas through patient data-driven analysis. We analyzed RNA sequencing and clinical data from publicly available tumor tissue samples of 8977 carcinoma patients in the Genomic Data Commons. Our findings revealed that <em>PTAFR</em> overexpression correlates with reduced patient survival, increased tumor size, and enhanced lymph node metastasis. Further analysis identified 151 differentially expressed genes associated with <em>PTAFR</em>, many of which regulate immune responses and proto-oncogenic signaling. Histological and single-cell analyses demonstrated an immunosuppressive TME in carcinoma tissues with elevated <em>PTAFR</em> expression. <em>In vivo</em> validation indicated reduced tumor growth and increased infiltration of pro-inflammatory cells in <em>PTAFR</em> knockout mice. Protein modeling suggests that PTAFR forms physical complexes with immunosuppressive mediators STAT3 and PDL2, and that pathogenic variants may disrupt the PAF-binding domain, potentially altering its signaling. Together, our findings establish PTAFR as a critical regulator of tumor progression, directly linking its expression to an immunosuppressive signaling in TME, enhanced tumor growth, and reduced patient survival, underscoring its potential as a therapeutic target.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114643"},"PeriodicalIF":3.3,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257625","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":"Role of GNL3L in lung cancer: Mediating proliferation and progression through NF-κB pathway activation and upregulation of Slug, MMP2, and MMP9","authors":"Qian Wang ,&nbsp;Xiao-Qi Zhang ,&nbsp;Shan-Shan Liu ,&nbsp;Xin-Yan Liu ,&nbsp;Xiao-Jing Lv ,&nbsp;Lei Zhang ,&nbsp;Hong Lv","doi":"10.1016/j.yexcr.2025.114630","DOIUrl":"10.1016/j.yexcr.2025.114630","url":null,"abstract":"<div><div>The precise involvement of Guanine Nucleotide-Binding Protein-Like 3-Like Protein (GNL3L) in lung cancer progression and invasion remains unclear. In this study, we explored the impact and underlying mechanisms of GNL3L on the proliferation, migration, and invasion of lung adenocarcinoma (LUAD), and evaluated the therapeutic potential of targeting GNL3L. Inhibition of GNL3L expression led to a notable decrease in the <em>in vitro</em> proliferation, migration, and invasion of A549 and H1299 non-small cell lung cancer (NSCLC) cells. Meanwhile, GNL3L silencing could significantly reduce the tumor volume of the nude mice and improve the outcomes of tumor-bearing mice <em>in vivo</em>. Additionally, inhibition of GNL3L expression dramatically suppressed NF-κB activation and Slug, MMP2, and MMP9 expression. Overexpression of Slug or treatment of the GNL3L-deficient cells with NF-κB activator can partially restore the growth suppressed by GNL3L deficiency, and combined treatment with Slug overexpression and NF-κB activator could totally restore the suppressed cell growth caused by GNL3L deficiency. Moreover, the overexpression of MMP2 or MMP9 could partially enhance the reduced migration and invasion caused by GNL3L deficiency, and this GNL3L-deficiency-caused suppression of migration and invasion can be totally restored by the overexpression of MMP2 and MMP9 together. These results strongly indicated that GNL3L has the capability to activate the NF-κB and increase Slug, MMP2, and MMP9 expression, which in turn could stimulate the proliferation, migration, and invasion of lung cancer cells. NF-κB activation and Slug, MMP2, and MMP9 expression enhanced by GNL3L, leading to the promotion of proliferation, migration, and invasion of lung cancer cells, indicating the therapeutic implications and potential significance of these pathways in the progression and invasion of NSCLCs that overexpress GNL3L protein.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114630"},"PeriodicalIF":3.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224877","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":"KLF15 deficiency contributes complement activation and podocyte injury in IgA nephropathy via regulating p300/ NF-κB axis","authors":"Weiyuan Lin ,&nbsp;Shanhong Shi ,&nbsp;Yanling Zheng ,&nbsp;Jiong Cui ,&nbsp;Jianxin Wan","doi":"10.1016/j.yexcr.2025.114631","DOIUrl":"10.1016/j.yexcr.2025.114631","url":null,"abstract":"<div><div>Krüppel-Like Factor 15 (KLF15) is a member of the Krüppel-like subfamily of zinc finger transcription factors, involved in a diverse renal physiology and diseases. The exact roles of KLF15 in IgA nephropathy (IgAN) have not been fully investigated. To address the issue of KLF15 expression and its exact roles in IgAN, IgAN mouse models and IgA-treated podocytes MPC-5 were established. Co-immunoprecipitation (Co-IP) assay was conducted to detect the interaction between KLF15 and p300. Levels of genes and complement factors were determined by Western blot, immunofluorescence, immunohistochemistry and ELISA assays. Podocytes apoptosis was detected with flow cytometry. KLF15 expression was downregulated in both renal tissues of IgAN mouse models and IgA-treated podocytes. This suppression coincided with elevated levels of complement components C3a and C5a, along with increased complement factor H (CFH) expression, collectively suggesting activation of the complement activation in IgA nephropathy. Besides, NF-κB was activated in IgAN, evidenced by the elevated levels of NF-κB p65 and its acetylation at lysine 310 as well as IκBα phosphorylation in IgAN models and IgA-treated podocyte. KLF15 overexpression alleviated complement activation and IgAN podocyte injury, characterized by improved cell viability, reduced apoptotic cells and apoptotic proteins expression (Bax/Bcl-2 and cleaved-caspase3), upregulated expression of nephrin and podocin, and suppressed complement components. In terms of mechanism, KLF15 overexpression could inhibit NF-κB activation by interacting with p300 to decrease p300 level, which was further confirmed by using p300 activator CTB or NF-κB activator PMA. These results indicate that KLF15 protects against podocyte injury in IgA nephropathy by suppressing complement system activation and modulating the p300/NF-κB signaling axis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114631"},"PeriodicalIF":3.3,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144212944","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":"Mechanical stretch-triggered EGR1 overexpression enhances macrophage M2 polarization and drives mitochondrial fission","authors":"Fei Han ,&nbsp;Yi Cheng ,&nbsp;Xianzhi Xu,&nbsp;Jiayi Yin,&nbsp;Wei-Bing Zhang","doi":"10.1016/j.yexcr.2025.114621","DOIUrl":"10.1016/j.yexcr.2025.114621","url":null,"abstract":"<div><div>Orthodontic tooth movement involves a complex interaction between mechanical forces and bone tissue remodeling. As a response to mechanical stimuli, macrophages play an important role in tissue remodeling and potential side effects. In this study, we investigated the molecular mechanism of macrophage polarization under mechanical stimulation, focusing on the dual regulation of EGR1 (Early Growth Response 1) in mitochondrial dynamics and macrophage polarization. In the cyclic stretch stress model of RAW264.7 cells in vitro, we found that mechanical tension promotes the M2 polarization phenotype of macrophages. During the first to second hour of mechanical stretching, the expression of iNOS, ARG-1, and CD163 in cells increased. At the same time, significant changes in macrophage mitochondrial dynamics include enhanced fission behavior and decreased membrane potential. The transcriptome sequencing results indicated that EGR1 was rapidly upregulated after mechanical stimulation and translocated from the cytoplasm to the nucleus. Inhibition of mitochondrial fission or knockdown of EGR1 significantly inhibited tension-induced M2 polarization. Moreover, this process may be associated with the PI3K-Akt signaling pathway. Our research findings reveal new insights into the connection between mechanical forces and macrophage function through EGR1-mediated mitochondrial dynamics. This work provides new perspectives on bone remodeling during orthodontic movement.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114621"},"PeriodicalIF":3.3,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208075","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":"Macrophage-derived microparticles facilitate the dissemination and spread of Japanese encephalitis virus and offer targets for antiviral intervention","authors":"Anjali Singh,&nbsp;Alok Kumar","doi":"10.1016/j.yexcr.2025.114618","DOIUrl":"10.1016/j.yexcr.2025.114618","url":null,"abstract":"<div><div>Japanese encephalitis virus (JEV) is thought to spread systemically; however, its transport and propagation mechanisms remain unclear. This study examined JEV progression through analysis of macrophage response and macrophage-derived microparticles (MPs) dynamics. MPs were isolated from conditioned media of macrophages at 72 h post-infection to assess their role in JEV transmission. Flow cytometry, qRT-PCR and western blotting were performed to analyze the MPs' JEV content and protein profiles. To further determine the impact of MPs on viral spread, MPs were neutralized and cocultured with uninfected macrophages. JEV infection was also mapped in the brain and lymph nodes at 24 h and 7 days post-infection to investigate early viral movement via macrophage-derived MPs. The findings indicate macrophage-derived MPs facilitate JEV transit from the brain to the lymph nodes. JEV infection of macrophages triggers apoptosis, increased viral replication, and a proinflammatory response, leading to the heightened secretion of MPs. These MPs carried JEV RNA, cytokines, and proteins such as HSP90 and flotillin-1. MPs from infected macrophages promoted viral spread to uninfected macrophages, initiating viremia. Neutralizing MPs with annexin V antibodies or heat inactivation significantly reduced JEV RNA levels in cocultures. These results suggest macrophage-derived MPs play a key role in JEV dissemination and presenting potential targets for antiviral intervention.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114618"},"PeriodicalIF":3.3,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198563","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 BMI1-Angiopoietin-2 axis as an independent prognostic factor in colorectal cancer","authors":"Yin-Chou Hsu ,&nbsp;Chi-Wen Luo ,&nbsp;Shu-Jyuan Chang ,&nbsp;Chiao-Ying Lai ,&nbsp;Yu-Tzu Yang ,&nbsp;Yi-Zi Chen ,&nbsp;Mei-Hsiang Hsu ,&nbsp;Cheuk-Kwan Sun ,&nbsp;Mei-Ren Pan","doi":"10.1016/j.yexcr.2025.114622","DOIUrl":"10.1016/j.yexcr.2025.114622","url":null,"abstract":"<div><h3>Background</h3><div>The polycomb group protein B-lymphoma Moloney murine leukemia virus Insertion region-1 (BMI1), a transcriptional repressor, has been implicated in colorectal cancer (CRC) progression. This study investigated the role of BMI1 in the regulation of angiogenesis and its association with angiopoietin 2 (ANGPT2) in CRC.</div></div><div><h3>Methods</h3><div>The highly metastatic CRC cell line SW620, known for its high BMI1 expression, was used to examine the effects of BMI1 knockdown and pharmacological inhibition using PTC209. Angiogenesis was assessed by tube formation and transendothelial migration assays. Quantitative real-time polymerase chain reaction <strong>(</strong>RT-qPCR) arrays were conducted to identify angiogenesis-related genes, and bioinformatics analysis using the TIMER database (version 2.0) was used to validate the correlation between BMI1 and angiogenic factors. Western blotting and immunohistochemistry confirmed protein-level interactions in cell and tissue samples. Clinicopathological associations were analyzed in 44 patients with advanced CRC, using survival analysis and multivariate regression models.</div></div><div><h3>Results</h3><div>BMI1 knockdown significantly reduced tube formation and endothelial cell adhesion in SW620 cells. RT-qPCR and database analyses revealed a strong positive correlation between BMI1 and ANGPT2 expression (r = 0.366, <em>p</em> &lt; 0.05). Protein-level analysis confirmed that BMI1 is essential for ANGPT2 expression, which was further validated in CRC clinical specimens and showed a significant correlation (<em>p</em> = 0.039). Survival analysis indicated that high BMI1 and ANGPT2 expression levels were significantly associated with poor overall survival and progression-free survival (<em>p</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>BMI1 promotes angiogenesis in CRC by upregulating ANGPT2 expression. High BMI1 and ANGPT2 levels served as independent prognostic factors for tumor progression, highlighting their potential as therapeutic targets for CRC management.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 1","pages":"Article 114622"},"PeriodicalIF":3.3,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191702","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":"SESN2 mediates resistance training-induced improvements in exercise performance and energy metabolism in C57BL/6J mice","authors":"Yating Huang ,&nbsp;Shiqi Sun ,&nbsp;Xuege Yang ,&nbsp;Xiuru Li ,&nbsp;Yanshuo Zhou ,&nbsp;Sujuan Liu ,&nbsp;Yanmei Niu ,&nbsp;Li Fu","doi":"10.1016/j.yexcr.2025.114617","DOIUrl":"10.1016/j.yexcr.2025.114617","url":null,"abstract":"<div><div>Long-term resistance training promotes skeletal muscle hypertrophy and boosts energy metabolism. The stress-inducible protein, SESN2 is a mediator of aerobic training benefits. However, whether SESN2 mediates resistance training to promote skeletal muscle hypertrophy and energy metabolism remains elusive. In this study, eight-week-old C57BL/6J male wild-type (WT) and SESN2^−/− mice were subjected to resistance training intervention for 12 weeks. Our results revealed that SESN2 deficiency weakened the effects of resistance training on the increase of grip strength, maximum load capacity, time to exhaustion, and grid suspension time. SESN2 promoted skeletal muscle hypertrophy by inhibiting protein degradation in response to resistance training. Moreover, SESN2 ablation blocked the resistance training-induced improvements in oxygen consumption, carbon dioxide production and energy expenditure. Glycolysis and tricarboxylic acid cycle in skeletal muscle of SESN2^−/− mice remain unchanged after resistance training. Furthermore, SESN2 deletion did not alter the expression of key metabolic enzymes in glycolysis and tricarboxylic acid cycle in both atrophied skeletal muscle and resistance exercise preconditioned muscle. These results imply that the SESN2 is a crucial regulator in facilitating the beneficial effects of resistance training on exercise performance, skeletal muscle mass and energy metabolism. This study contributes to the understanding of the mechanisms by which resistance training promotes skeletal muscle energy metabolism.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 1","pages":"Article 114617"},"PeriodicalIF":3.3,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138400","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":"Decoding the function of cancer-associated fibroblasts in osteosarcoma: Molecular pathways, therapeutic approaches and prognostic significance","authors":"Chou-Yi Hsu ,&nbsp;Ali G. Alkhathami ,&nbsp;Thanaa amir ahmed ,&nbsp;Muktesh Chandra ,&nbsp;Jaafaru Sani Mohammed ,&nbsp;H. Malathi ,&nbsp;Krishan Kumar Sah ,&nbsp;Ashish Singh Chauhan ,&nbsp;Ahmad iwadi ,&nbsp;Abbas Fadhel Ali","doi":"10.1016/j.yexcr.2025.114612","DOIUrl":"10.1016/j.yexcr.2025.114612","url":null,"abstract":"<div><div>Herein, we summarize the latest insights into osteosarcoma, the most prevalent primary malignant bone tumor, known for its aggressive nature, poor outcome, and especially poor prognosis when metastasis develops. Given recent research implicating the crucial role of the tumor microenvironment (TME) in osteosarcoma progression, cancer-associated fibroblasts (CAFs) emerged as key players. Through the secretion of cytokines, remodeling of the extracellular matrix (ECM), and cross-talk with osteosarcoma cells, CAFs collectively promote tumor growth, metastasis, and immune evasion. Exosomes derived from CAFs, which could also serve as important mediators of osteosarcoma progression, have been found to transport oncogenic lncRNAs like SNHG17 and linc00881. Moreover, some subtypes of CAFs, such as TOP2A + CAFs, have shown significant prognostic value for tumor aggressiveness. Thus, targeted CAFs was identified as a promising therapeutic modality, with strategies such as fibroblast activation protein (FAP) inhibition, TGF-β blockade, and CXCL12/CXCR4 axis inhibition demonstrating positive outcomes in preclinical models. The combination of CAF-targeted therapies with immunotherapies or chemotherapy has shown additional potential to reverse this CAF-induced resistance. Autophagy regulation in CAFs can be therapeutic opportunities for novel Interevent strategies.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 1","pages":"Article 114612"},"PeriodicalIF":3.3,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126961","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":"Novel approaches to 3D cancer heterospheroid culture and assay development for immunotherapy screening","authors":"Natasha Helleberg Madsen ,&nbsp;Boye Schnack Nielsen ,&nbsp;Isabella Skandorff ,&nbsp;Carlos Rodriguez-Pardo ,&nbsp;Sine Reker Hadrup ,&nbsp;Maria Ormhøj ,&nbsp;Kim Holmstrøm ,&nbsp;Jesper Larsen ,&nbsp;Monika Gad","doi":"10.1016/j.yexcr.2025.114604","DOIUrl":"10.1016/j.yexcr.2025.114604","url":null,"abstract":"<div><div>Advanced 3D heterospheroids, composed of cancer, fibroblast, and immune cells, serve as more physiologically relevant models for anticancer drug screening and immunotherapy research compared to traditional 2D cultures. This study aimed to optimize the culturing, dissociation, and analysis of heterospheroids, addressing limitations that restrict their broader use in immunotherapy research. Our study revealed significant effects of Human Plasma-Like culture medium on cell viability, necrotic core formation, and the spatial organization of cancer and fibroblast cells within heterospheroids compared to DMEM and RPMI media. In HT-29 heterospheroids, cell viability decreased from 75 % in DMEM to 20 % in HPLM, which was accompanied by increased necrotic core formation and elevated PD-L1 expression. TrypLE™ effectively dissociated heterospheroids but compromised immune cell viability and surface marker detection. In comparison, Accutase™ significantly reduced cell yield, while collagenase I preserved immune cell markers but affected those on cancer cells. Furthermore, we developed a luciferase-based assay to measure immune-mediated cancer cell killing in heterospheroids, excluding signals from non-target cells, such as dying fibroblasts and immune cells, without requiring spheroid lysis or dissociation. Our findings highlight the importance of tailoring experimental conditions to reflect specific tumor characteristics, thus enhancing the utility of heterospheroids in drug discovery and immunotherapy research.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 2","pages":"Article 114604"},"PeriodicalIF":3.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086057","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 “ANGPTL8/betatrophin alleviates insulin resistance via the Akt-GSK3βor Akt-FoxO1 pathway in HepG2 cells” [Exp. Cell Res., 2016 Jul 15;345(2):158-67.doi: 10.1016/j.yexcr.2015.09.012. Epub 2015 Sep 24]","authors":"Xing Rong Guo ,&nbsp;Xiao Li Wang ,&nbsp;Yun Chen ,&nbsp;Ya Hong Yuan ,&nbsp;Yong Mei Chen ,&nbsp;Yan Ding ,&nbsp;Juan Fang ,&nbsp;Liu Jiao Bian ,&nbsp;Dong Sheng Li","doi":"10.1016/j.yexcr.2025.114601","DOIUrl":"10.1016/j.yexcr.2025.114601","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"449 1","pages":"Article 114601"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076906","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}