Experimental cell research最新文献

{"title":"RhFGF21 protected PC12 cells against mitochondrial apoptosis triggered by H2O2 via the AKT-mediated ROS signaling pathway","authors":"Jingjing Lin ,&nbsp;Junyi Wu ,&nbsp;Yifan Xu ,&nbsp;Yeli Zhao ,&nbsp;Shasha Ye","doi":"10.1016/j.yexcr.2025.114417","DOIUrl":"10.1016/j.yexcr.2025.114417","url":null,"abstract":"<div><div>One of the pathological mechanisms of neurodegenerative diseases is that oxidative stress damages neurons. Therefore, reducing reactive oxygen species (ROS) overload may be a promising approach for preventing and treating neurological diseases. Fibroblast growth factor 21 (FGF21) is crucial for protecting and restoring various forms of pathological injury. Consequently, the operating mechanism of FGF21 was investigated. Our research revealed that rhFGF21 could enhance the cell viability by alleviating the damage to PC12 cells after H₂O₂ action of via mechanisms decreasing mitochondrial apoptosis, reducing ROS production, increasing antioxidant enzyme levels, adenosine triphosphate (ATP) synthesis and mitochondrial membrane potential (MMP). Excessive ROS trigger cell apoptosis. Our findings revealed that tBHP counteracted the cell viability-boosting effect of rhFGF21 in H₂O₂-stimulated PC12 cells, whereas N-acetyl-L-cysteine (NAC) enhanced the viability-promoting effect of rhFGF21 in these cells. AKT is crucial in mediating ROS-induced cell apoptosis. The treatment of PC12 cells exposed to H₂O₂ with rhFGF21 resulted in upregulation of p-AKT expression. Moreover, rhFGF21 inhibited ROS levels and increased the cell viability, which were both reversed by administration of an AKT inhibitor (wortmannin). The research discovered that rhFGF21 mitigated mitochondrial apoptosis in PC12 cells exposed to H₂O₂ through the functioning of the AKT and ROS signaling axis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114417"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964373","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":"SOX11 silence inhibits atherosclerosis progression in ApoE-deficient mice by alleviating endothelial dysfunction","authors":"Yanhui Ni ,&nbsp;Jingjing Cao ,&nbsp;Yuxuan Li ,&nbsp;Xiaoyong Qi","doi":"10.1016/j.yexcr.2025.114422","DOIUrl":"10.1016/j.yexcr.2025.114422","url":null,"abstract":"<div><div>SRY-Box Transcription Factor-11 (SOX11) is a transcriptional regulatory factor that plays a crucial role in inflammatory responses. However, its involvement in atherosclerosis (AS), a cardiovascular disease driven by endothelial cell inflammation, remains unknown. This study aims to elucidate the role of SOX11 in AS. The expression of SOX11 was found to be elevated in the aortic tissue of AS mice induced by feeding ApoE-deficient mice a high-fat diet. Knockdown of SOX11 using lentiviral-mediated SOX11-specific shRNA via tail vein injection resulted in a reduction in plaque area and lipid deposition within plaques at the aortic root. Furthermore, silencing SOX11 led to decreased expression of cell adhesion factors Intercellular Cell Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1, as well as reduced levels of inflammatory factors Interleukin (IL)-6, IL-1β, and chemokine Monocyte Chemotactic Protein-1. In the human umbilical vein endothelial cells (HUVECs) induced by Tumor Necrosis Factor (TNF)-α, increased inflammation was observed at the cellular level, along with enhanced monocyte adhesion. Infection of HUVECs with lentivirus carrying specific shRNA targeting SOX11 inhibited inflammatory response. Mechanistically, chromatin immunoprecipitation (ChIP)-PCR results revealed that SOX11 bound to the promoters of downstream target genes Tumor Necrosis Factor Receptor-Associated Factor-1 (TRAF1), Cluster of Differentiation (CD)40, and CD36, positively regulating their transcription. In conclusion, SOX11 plays a pivotal role in promoting endothelial cell inflammation. Suppression of SOX11 reduces endothelial cell inflammation by inhibiting the transcription of TRAF1, CD40, and CD36, thereby impeding the progression of atherosclerosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114422"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142977773","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":"OTUB1 mediates PARP1 deubiquitination to alleviate NAFLD by regulating HMGB1","authors":"Shuhua Ai ,&nbsp;Juanli Pan ,&nbsp;Qi Liu ,&nbsp;Fenfen Tang ,&nbsp;Ting Wen ,&nbsp;Yulin Yuan ,&nbsp;Qunjun He ,&nbsp;Lu Huang","doi":"10.1016/j.yexcr.2025.114425","DOIUrl":"10.1016/j.yexcr.2025.114425","url":null,"abstract":"<div><div>Nonalcoholic fatty liver disease (NAFLD) is a common chronic disease characterized by hepatocyte steatosis, which excludes alcohol, drugs and other definite liver damage-related factors. It has been reported that OTUB1 serves a significant role in the regulation of glucose and lipid metabolism. The present study aimed to investigate the molecular mechanism underlying the effect of OTUB1 on regulating NAFLD. The NAFLD mouse model was induced via high-fat-diet, and glucose and insulin tolerance tests were then performed. In addition, the serum levels of total cholesterol (TC) and triglycerides (TG) were detected. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were assessed using the corresponding biochemical assays. Hematoxylin and eosin, and periodic acid-Schiff staining was carried out to evaluate the liver pathology in mice. The expression levels of the NAFLD-related genes and inflammatory genes were determined by reverse transcription-quantitative PCR, Western blot analysis and immunofluorescence staining. Furthermore, the regulatory association between OTUB1 and poly (adenosine diphosphate-ribose) polymerase (PARP)-1 was assessed by co-immunoprecipitation assay. The results showed that OTUB1 was significantly upregulated in both in vitro and in vivo NAFLD models. Knockout of OTUB1 significantly improved affected glucose tolerance and insulin sensitivity, decreased TG and TC content, and decreased ALT, AST and ALP levels. In addition, the results show that OTUB1 can regulate the expression of PARP1 by inhibiting the ubiquitination of PARP1, while PARP1 knockout can inhibit liver inflammation by regulating HMGB1, thereby improving NAFLD. Targeting OTUB1 could be a potential therapeutic strategy for the NAFLD.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114425"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002906","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":"Unraveling the role of SSH1 in chronic neuropathic pain: A focus on LIMK1 and Cofilin Dephosphorylation in the prefrontal cortex","authors":"Hui Zhang ,&nbsp;XiaoJing Zhai ,&nbsp;WenWen Zhang ,&nbsp;Yu He ,&nbsp;BeiBei Yu ,&nbsp;He Liu ,&nbsp;XiaoWen Meng ,&nbsp;FuHai Ji","doi":"10.1016/j.yexcr.2024.114383","DOIUrl":"10.1016/j.yexcr.2024.114383","url":null,"abstract":"<div><h3>Background and objective</h3><div>Neuropathic pain, a debilitating condition stemming from nervous system injuries, has profound impacts on quality of life. The medial prefrontal cortex (mPFC) plays a crucial role in the modulation of pain perception and emotional response. This study explores the involvement of Slingshot Homolog 1 (SSH1) protein in neuropathic pain and related emotional and cognitive dysfunctions in a mouse model of spared nerve injury (SNI).</div></div><div><h3>Methods</h3><div>SNI was induced in C57BL/6J mice. SSH1's role was investigated via its overexpression and knockdown using lentiviral vectors in the mPFC. Behavioral assays (thermal and mechanical allodynia, open field test, elevated plus maze, tail suspension test, Y-maze, and novel object recognition were conducted to assess pain sensitivity, anxiety, depression, and cognitive function. Tissue samples underwent Hematoxylin and Eosin staining, Western blotting, immunofluorescence, co-immunoprecipitation, and enzyme-linked immunosorbent assay for inflammatory markers.</div></div><div><h3>Results</h3><div>SNI mice displayed significant reductions in neuronal density and dendritic integrity in the mPFC, alongside heightened pain perception and emotional disturbances, as compared to sham controls. Overexpression of SSH1 ameliorated these alterations, improving mechanical and thermal thresholds, reducing anxiety and depressive behaviors, and enhancing cognitive performance. Conversely, SSH1 knockdown exacerbated these phenotypes. Molecular investigations revealed that SSH1 modulates pain processing and neuronal health in the mPFC partially through the dephosphorylation of Cofilin and LIM domain kinase 1 (LIMK1), as evidenced by changes in their phosphorylation states and interaction patterns.</div></div><div><h3>Conclusion</h3><div>SSH1 plays a pivotal role in the modulation of neuropathic pain and associated neuropsychological disturbances in the mPFC of mice. Manipulating SSH1 expression can potentially reverse the neurophysiological and behavioral abnormalities induced by SNI, highlighting a promising therapeutic target for treating neuropathic pain and its complex comorbidities.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114383"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863044","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":"Analyzing the functions of Translationally controlled tumor protein2 during growth, development and autophagy of Dictyostelium discoideum","authors":"Chanchal Choudhary,&nbsp;Bhavya Jain,&nbsp;Shweta Saran","doi":"10.1016/j.yexcr.2024.114400","DOIUrl":"10.1016/j.yexcr.2024.114400","url":null,"abstract":"<div><div>Translationally controlled tumor protein (TCTP) is a well conserved and ubiquitously expressed multifunctional protein found in many organisms and is involved in many pathophysiological processes like cell proliferation, differentiation, development and cell death. The role of TCTP in anti-apoptosis and cancer metastasis makes it a promising candidate for cancer therapy. <em>Dictyostelium discoideum,</em> a protist, has two isoforms (TCTP1 and TCTP2, now referred to as TPT1 and TPT2) of which we have earlier elucidated TPT1. Here, we analyzed the role of TPT2 in this organism. <em>tpt2</em> transcript was present throughout growth and development and is localized in the prestalk/stalk regions of multicellular structures developed. <em>tpt2</em> gene was disrupted with a BSR cassette using a double homologous recombination method. Disruption of <em>tpt2</em> gene (<em>tpt2‾</em>) exhibit reduced cell proliferation and nutrient-uptake. Additionally, development in <em>tpt2‾</em> was delayed by 2 h, formed small-sized aggregates that developed into stalky fruiting bodies with reduced spore viability. In contrast, overexpressed <em>tpt2</em> (<em>tpt2</em>^<em>OE</em>) showed increased cell proliferation and development, formed large-size aggregates that developed into spory fruiting bodies with increased spore viability. TPT2 regulates prestalk/prespore ratio and cell-type differentiation as abrogation of <em>tpt2</em> gene resulted in altered localization of cell-type markers and an inclination towards the prestalk/stalk pathway while <em>tpt2</em>^<em>OE</em> showed a prespore/spore biasness when mixed with wild-type cells. Deletion of either <em>tpt1</em> or <em>tpt2</em> gene showed increased autophagic flux indicating their involvement in negative regulation of autophagy. This study provides insights into the intricate involvement of TCTP in cellular dynamics and development of <em>D. discoideum.</em></div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114400"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926968","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":"IGSF8 impairs migration and invasion of trophoblast cells and angiogenesis in preeclampsia","authors":"Xiaodan Chu,&nbsp;Xuan Chen,&nbsp;Man Guo,&nbsp;Xinyue Li,&nbsp;Zhihai Qu,&nbsp;Peiling Li","doi":"10.1016/j.yexcr.2025.114405","DOIUrl":"10.1016/j.yexcr.2025.114405","url":null,"abstract":"<div><div>Insufficient trophoblast cell infiltration is implicated in the progression of preeclampsia (PE). The immunoglobulin superfamily member 8 (IGSF8) has been shown to promote cell migration, invasion, and epithelial mesenchymal transition (EMT). However, the specific impact of IGSF8 on trophoblast cells in PE has not been definitively demonstrated. To address this, placental tissues from PE patients and normal subjects was collected. A PE-like rat model was established by administering L-NAME (60 mg/kg) intragastrically to pregnant rats from the 10th to the 19th day of gestation. Knockdown and overexpression plasmids of IGSF8 were transfected into JEG-3 cells for further experiments. Clinical samples indicated impaired spiral artery remodeling, and high IGSF8 expression in the placental tissues of PE patients. PE rats exhibited increased mean arterial pressure, elevated 24-h urine protein levels, higher abortion rates, and decreased placental and fetal weight compared to rats of sham group. Failure of physiological transformation of spiral arteries was observed in PE rats, along with increased IGSF8 expression. IGSF8 overexpression inhibited JEG-3 cell migration, invasion and EMT, as well as reduced release of VEGF in JEG-3 cells, impairing HUVEC tube formation. mRNA-sequencing analysis of JEG-3 cells transfected with shIGSF8 showed differentially expressed genes related to angiogenesis, and mesenchymal cell differentiation, with IGSF8 knockdown being associated with the activation of pathways involved in blood vessel development and cell migration. Overall, this study suggests that IGSF8 plays a role in the development of PE and provides new insights for potential treatments.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114405"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926969","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":"Matrix-mediated activation of murine fibroblast-like synoviocytes","authors":"Isabel Zeinert ,&nbsp;Luisa Schmidt ,&nbsp;Till Baar ,&nbsp;Giulio Gatto ,&nbsp;Anna De Giuseppe ,&nbsp;Adelheid Korb-Pap ,&nbsp;Thomas Pap ,&nbsp;Esther Mahabir ,&nbsp;Frank Zaucke ,&nbsp;Bent Brachvogel ,&nbsp;Marcus Krüger ,&nbsp;Thomas Krieg ,&nbsp;Beate Eckes","doi":"10.1016/j.yexcr.2025.114408","DOIUrl":"10.1016/j.yexcr.2025.114408","url":null,"abstract":"<div><div>Fibroblast-like synoviocytes (FLS) are key cells promoting cartilage damage and bone loss in rheumatoid arthritis (RA). They are activated to assume an invasive and migratory phenotype. While mechanisms of FLS activation are unknown, evidence suggests that pre-damaged extracellular matrix (ECM) of the cartilage can trigger FLS activation. Integrin α11β1 might be involved in the activation, as it is increased in RA patients and hTNFtg mice, an RA mouse model.</div><div>We treated murine chondrocytes with TNFα to produce a damaged, RA-like matrix. Comparison to healthy chondrocyte matrix revealed decreased ECM proteins, e.g. collagens and proteoglycans, increased matrix-degrading proteins and elevated levels of inflammatory cytokines.</div><div>FLS responded to the damaged chondrocyte matrix with a matrix-remodeling and pro-inflammatory phenotype characterized by a gene signature involved in matrix degradation and increased production of CLL11 and CCL19. Damaged chondrocyte matrix stimulated increased <em>Itga11</em> expression in FLS, correlating with the increased α11β1 amounts in RA patients. FLS deficient in integrin α11β1 released lower amounts of inflammation-associated cytokines.</div><div>Our results demonstrate differences in healthy and RA-like chondrocyte ECM and distinctly different responses of wt FLS to damaged versus healthy ECM.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114408"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA circPFKP suppress gastric cancer progression through targeting miR-346/CAMD3 axis","authors":"Xin Song ,&nbsp;Guochao Zhang ,&nbsp;Jinwei Niu,&nbsp;Haibin Liu,&nbsp;Chaofeng Li,&nbsp;Wu Ning,&nbsp;Lei Zhou","doi":"10.1016/j.yexcr.2024.114390","DOIUrl":"10.1016/j.yexcr.2024.114390","url":null,"abstract":"<div><div>Studies have demonstrated that circular RNAs (circRNAs) exert an important regulatory function in the pathogenesis of various tumors. However, their role in gastric cancer (GC) is still not completely understood. In our study, the differentially expressed circRNAs in GC tissues and matched adjacent normal tissues were analyzed by utilizing gene chips GSE93541, GSE89143, and GSE78092. The expression of has_circ_0006608 (circPFKP), miR-346, and CAMD3 was analyzed through quantitative real-time polymerase chain reaction (qRT-PCR). The CCK-8 assay and Transwell assay were employed to detect the effect of circPFKP on the proliferation, migration, and invasion of gastric cancer cells. The mice xenograft assay was used to assess the function of circPFKP in vivo. The targeting relationship between circPFKP, miR-346, and CAMD3 was predicted by bioinformatics analysis and confirmed by the dual-luciferase reporter assay and RNA pull-down assay. Our results screened and verified that circPFKP was down-regulated in gastric cancer tissues and cells. Overexpression of circPFKP in GC cells can inhibit cell proliferation, migration, invasion, and tumor growth in vivo. Additionally, circPFKP has been shown to act as a sponge for miR-346 to modulate the expression of CAMD3. Finally, we demonstrated that overexpression of CAMD3 or miR-346 inhibitor significantly reversed the effects of si-circPFKP on the proliferation, migration, and invasion of gastric cancer cells. In conclusion, this study provided that circPFKP inhibits the progression of GC via the miR-346/CAMD3 axis, this may provide a noval biomarker for the diagnosis and treatment of GC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114390"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921404","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":"Cancer-associated fibroblast-derived exosomes in cancer progression: A focus on hepatocellular carcinoma","authors":"Chou-Yi Hsu ,&nbsp;Abdulrahman T. Ahmed ,&nbsp;Safia Obaidur Rab ,&nbsp;Subasini Uthirapathy ,&nbsp;Suhas Ballal ,&nbsp;Rishiv Kalia ,&nbsp;Renu Arya ,&nbsp;Deepak Nathiya ,&nbsp;Muthena kariem ,&nbsp;Abed J. Kadhim","doi":"10.1016/j.yexcr.2025.114424","DOIUrl":"10.1016/j.yexcr.2025.114424","url":null,"abstract":"<div><div>The tumor microenvironment (TME) has drawn much interest recently in the search for innovative cancer therapeutics, especially in light of the growing body of evidence supporting the efficacy of immune checkpoint inhibitors (ICIs). The TME comprises various cell types within the extracellular matrix (ECM), such as immune cells, endothelial cells, and cancer-associated fibroblasts (CAFs). Throughout the malignancy, these cells interact with cancerous cells and with one another. Inside the TME, CAFs are predominant and diverse cell types essential in regulating immune escape, angiogenesis, chemotherapeutic resistance, and cancer cells to invade and metastasize. Extracellular vesicles (EVs) and soluble substances are secreted by CAFs, which also remodel the extracellular matrix to partially coordinate their actions. A subclass of EVs called exosomes comprises proteins, lipids, and nucleic acids. Exosomes contain macromolecules that can transfer from one cell to another, changing the recipient cell's activity. Since exosomes are also circulating, it is possible to investigate their composition as potential biomarkers for cancer patient's diagnosis and prognosis. In this review, we focus on the function of exosomes derived from CAFs in the communications between CAFs and other TME cells and cancerous cells. Initially, we explain the various roles of CAFs in carcinogenesis. Subsequently, we address the processes by which CAFs interact with hepatocellular carcinoma (HCC) cells and other cells within the TME, with a special focus on the function of exosomes. We then go into greater detail regarding the processes by which exosomes derived from CAFs aid in the development of HCC, in addition to the clinical implications of exosomes. Finally, we address facets of exosomes that warrant additional research, such as novel discoveries regarding the enhancement of immune checkpoint inhibitor blockade therapy.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114424"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143002905","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":"Exploring the role of exosomal lncRNA in cancer immunopathogenesis: Unraveling the immune response and EMT pathways","authors":"Sharif Alhajlah ,&nbsp;Saade Abdalkareem Jasim ,&nbsp;Farag M.A. Altalbawy ,&nbsp;Pooja Bansal ,&nbsp;Harpreet Kaur ,&nbsp;Jaafaru Sani Mohammed ,&nbsp;Mohammed N. Fenjan ,&nbsp;Reem Turki Edan ,&nbsp;M.K. Sharma ,&nbsp;Ahmed Hussein Zwamel","doi":"10.1016/j.yexcr.2024.114401","DOIUrl":"10.1016/j.yexcr.2024.114401","url":null,"abstract":"<div><div>Exosomes are membrane-bound vesicles secreted by diverse cell types, serving as crucial mediators in intercellular communication and significantly influencing cancer development. Exosomes facilitate complex signaling processes in the tumor microenvironment for immunomodulation, metastasis, angiogenesis, and treatment resistance. Notably, long non-coding RNAs (lncRNAs), a class of non-coding RNAs, engage with mRNA, DNA, proteins, and miRNAs to modulate gene expression through multiple mechanisms, including transcriptional, post-transcriptional, translational, and epigenetic pathways. The quantitative dynamics of exosomal lncRNAs show a consistent variation correlating with cancer progression and metastasis, suggesting their potential utility as biomarkers for cancer diagnosis and prognosis. Additionally, exosomal lncRNAs can yield critical insights into therapeutic responses in patients. The identification of exosomal lncRNAs as indicators for various cancer subtypes presents them not only as prognostic tools but also as promising therapeutic targets. Despite their potential, the precise functions of exosomal lncRNAs in the cancer biology landscape remain inadequately understood. This paper delves into the multifaceted roles of exosomal lncRNAs, particularly in the context of breast cancer, highlighting their promise for therapeutic applications. A thorough comprehension of exosomal lncRNAs is imperative for advancing our knowledge of the underlying mechanisms of breast cancer, ultimately paving the way for the development of more effective treatment strategies for patients.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"445 1","pages":"Article 114401"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909459","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}