Experimental cell research最新文献

lncRNA NR_146969 promotes the progression of lung adenocarcinoma

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-25 DOI: 10.1016/j.yexcr.2025.114535

Ying Chen , Juan Wang , Linguo Gu , Hongzuo Chen , Zhengling Gai , Rui Hu , Bei Qing , Yunchang Yuan , Zhenkun Xia

{"title":"lncRNA NR_146969 promotes the progression of lung adenocarcinoma","authors":"Ying Chen , Juan Wang , Linguo Gu , Hongzuo Chen , Zhengling Gai , Rui Hu , Bei Qing , Yunchang Yuan , Zhenkun Xia","doi":"10.1016/j.yexcr.2025.114535","DOIUrl":"10.1016/j.yexcr.2025.114535","url":null,"abstract":"<div><h3>Background</h3><div>Emerging research suggests that dysregulation of long non-coding RNAs (lncRNAs) is closely linked to the onset and progression of cancer. In this study, we used lncRNA array technology to identify differentially expressed lncRNAs in lung adenocarcinoma patients and normal lung tissues. The study further explored the clinical significance and function of candidate lncRNAs in lung adenocarcinoma (LUAD). The results showed that lncRNA NR_146969 was upregulated in LAUD specimens and was associated with lymph node metastasis and clinical staging in LUAD patients.</div></div><div><h3>Methods</h3><div>The biological functions of lncRNA NR_146969 were observed using CCK-8, colony formation, transwell assay and xenograft tumor model. Explore the potential mechanism of action of lncRNA NR_146969 by FISH, dual luciferase reporter assay and recovery assay.</div></div><div><h3>Results</h3><div>Overall, lncRNA NR_146969 plays an oncogenic role in LUAD. Mechanically, lncRNA NR_146969 targets SLC6A14 via miR-26a-1-3p, leading to phosphorylation of the AKT/mTOR pathway, which promotes LUAD growth and metastasis.</div></div><div><h3>Conclusion</h3><div>Therefore, targeting lncRNA NR_146969 may provide a new therapeutic strategy for LUAD.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114535"},"PeriodicalIF":3.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143726238","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}

引用次数: 0

Irradiation of 125I seeds blocks glycolysis in pancreatic cancer by inhibiting KLF5 m6A methylation through the suppression of RBM15.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-25 DOI: 10.1016/j.yexcr.2025.114538

Jianjun Song, Fuping Kang, Xiaoning Chang, Jing Wu, Peng Zhang, Xiaolong Wang, Feng Wang

{"title":"Irradiation of 125I seeds blocks glycolysis in pancreatic cancer by inhibiting KLF5 m6A methylation through the suppression of RBM15.","authors":"Jianjun Song, Fuping Kang, Xiaoning Chang, Jing Wu, Peng Zhang, Xiaolong Wang, Feng Wang","doi":"10.1016/j.yexcr.2025.114538","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114538","url":null,"abstract":"<p><p>This paper investigated whether 125I seed irradiation for pancreatic cancer treatment was mediated through the RBM15/KLF5 pathway in glycolysis. The study collected peripheral blood from pancreatic cancer patients, and detected the expression of RBM15 and KLF5 expression in the serum of pancreatic cancer patients before and after 125I seed irradiation. An in vitro study was conducted to investigate the effects 125I seed irradiation on the malignant behavior and glycolysis of pancreatic cancer cells were explored. The underlying mechanisms were thoroughly examined through a series of logical experiments, including Western blot analysis, Dot-blot experiment, methylated RNA immunoprecipitation assay, and RNA pull down assay. A xenograft tumor model in nude mice was established and treated with 125I seed irradiation, which was employed to research the in vivo effect and mechanism of 125I seed irradiation for pancreatic cancer. The overexpressed RBM15 and KLF5 in serum of pancreatic cancer patients were reduced after 125I seed treatment. 125I seed treatment impaired pancreatic cancer cell proliferation and invasion; enhanced apoptosis; attenuated glycolysis; and reduced RBM15 and KLF5 expression. RBM15 overexpression partially reversed these influences of 125I seed treatment on pancreatic cancer cells. RBM15 was capable of increasing KLF5 expression, which might be achieved by promoting m6A methylation of KLF5. In vivo, 125I seed treatment blocked the growth of pancreatic cancer cells and decreased RBM15 and KLF5 expression in xenograft tumor, whereas RBM15 overexpression abolished these effects. 125I seed irradiation suppressed glycolysis in pancreatic cancer by inhibiting KLF5 m6A methylation through down-regulation of RBM15. This discovery establishes a solid foundation for the use of in the treatment of pancreatic cancer.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114538"},"PeriodicalIF":3.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729403","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}

引用次数: 0

Flavonoids in the regulation of microglial-mediated neuroinflammation; focus on fisetin, rutin, and quercetin.

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-25 DOI: 10.1016/j.yexcr.2025.114537

Mohannad Hamid Jasim, Rosull Saadoon Abbood, Gaurav Sanghvi, R Roopashree, Subasini Uthirapathy, Aditya Kashyap, A Sabarivani, Subhashree Ray, Yasser Fakri Mustafa, Hatif Abdulrazaq Yasin

{"title":"Flavonoids in the regulation of microglial-mediated neuroinflammation; focus on fisetin, rutin, and quercetin.","authors":"Mohannad Hamid Jasim, Rosull Saadoon Abbood, Gaurav Sanghvi, R Roopashree, Subasini Uthirapathy, Aditya Kashyap, A Sabarivani, Subhashree Ray, Yasser Fakri Mustafa, Hatif Abdulrazaq Yasin","doi":"10.1016/j.yexcr.2025.114537","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114537","url":null,"abstract":"<p><p>Neuroinflammation is a critical mechanism in central nervous system (CNS) inflammatory disorders, encompassing conditions such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis (MS), traumatic brain injury (TBI), encephalitis, spinal cord injury (SCI), and cerebral stroke. Neuroinflammation is characterized by increased blood vessel permeability, leukocyte infiltration, glial cell activation, and elevated production of inflammatory mediators, such as chemokines and cytokines. Microglia act as the resident macrophages of the central nervous system, serving as the principal defense mechanism in brain tissue. After CNS injury, microglia modify their morphology and downregulate genes that promote homeostatic functions. Despite comprehensive transcriptome analyses revealing specific gene modifications in \"pathological\" microglia, microglia's precise protective or harmful functions in neurological disorders remain insufficiently comprehended. Accumulating data suggests that the polarization of microglia into the M1 proinflammatory phenotype or the M2 antiinflammatory phenotype may serve as a sensible therapeutic strategy for neuroinflammation. Flavonoids, including rutin, fisetin, and quercetin, function as crucial chemical reservoirs with unique structures and diverse actions and are extensively used to modulate microglial polarization in treating neuroinflammation. This paper highlights the detrimental effects of neuroinflammation seen in neurological disorders such as stroke. Furthermore, we investigate their therapeutic benefits in alleviating neuroinflammation via the modulation of macrophage polarization.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114537"},"PeriodicalIF":3.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729399","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}

引用次数: 0

CMTM4 promotes PD-L1-mediated macrophage apoptosis by enhancing STAT2 phosphorylation in sepsis

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-22 DOI: 10.1016/j.yexcr.2025.114519

Feng Qi , Zhujun Yi , Yan Liu , Degong Jia , Hui Zhao , Gang Jiang , Jianping Gong

{"title":"CMTM4 promotes PD-L1-mediated macrophage apoptosis by enhancing STAT2 phosphorylation in sepsis","authors":"Feng Qi , Zhujun Yi , Yan Liu , Degong Jia , Hui Zhao , Gang Jiang , Jianping Gong","doi":"10.1016/j.yexcr.2025.114519","DOIUrl":"10.1016/j.yexcr.2025.114519","url":null,"abstract":"<div><h3>Background</h3><div>Macrophage apoptosis is a key contributor to the elimination of immune cells and increased susceptibility during sepsis. CKLF like MARVEL transmembrane domain containing 4 (CMTM4) is a membrane protein with four transmembrane domains. It has recently been implicated in the regulation of immune cell biological functions. However, its role in regulating macrophage apoptosis during sepsis has not been extensively studied.</div></div><div><h3>Methods</h3><div>Clinical samples were analyzed to determine CMTM4 expression levels and their correlation with clinical examination results. An in vitro model was developed using C57BL/6 mice and the THP-1 cell line. An immunofluorescence analysis was used to assess protein expression levels, apoptosis, and protein co-localization. Western blotting (WB) was used to measure protein expression levels, while flow cytometry was used to detect cell apoptosis. Transcriptomic sequencing was conducted to identify differentially expressed genes and to perform a functional enrichment analysis. Transcription factors were screened using databases. Chromatin immunoprecipitation, followed by quantitative PCR (ChIP-qPCR), was conducted to analyze protein–DNA interactions, and co-immunoprecipitation (Co-IP) was used to examine protein–protein interactions.</div></div><div><h3>Results</h3><div>CMTM4 expression in macrophages was upregulated in sepsis. The inhibition of CMTM4 expression reduced macrophage apoptosis. PD-L1 was identified as a key molecule regulated by CMTM4 in macrophage apoptosis. CMTM4 regulates PD-L1 by promoting the phosphorylation of its transcription factor, STAT2, rather than directly binding to PD-L1.</div></div><div><h3>Conclusion</h3><div>In sepsis, CMTM4 facilitates PD-L1-dependent macrophage apoptosis by enhancing STAT2 phosphorylation. This discovery offers new insights for the diagnosis and treatment of sepsis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114519"},"PeriodicalIF":3.3,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691507","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}

引用次数: 0

CTPS cytoophidia in Drosophila: distribution, regulation, and physiological roles

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-22 DOI: 10.1016/j.yexcr.2025.114536

Qingyi Wang , Ji-Long Liu , Jingnan Liu

{"title":"CTPS cytoophidia in Drosophila: distribution, regulation, and physiological roles","authors":"Qingyi Wang , Ji-Long Liu , Jingnan Liu","doi":"10.1016/j.yexcr.2025.114536","DOIUrl":"10.1016/j.yexcr.2025.114536","url":null,"abstract":"<div><div>Intracellular compartmentalization plays a critical role in maintaining cellular homeostasis and regulating metabolic processes. A growing body of evidence suggests that various metabolic enzymes, including CTP synthase (CTPS), can dynamically assemble into membraneless filamentous structures. The formation of these membraneless organelles is precisely regulated by the cellular metabolic state. CTPS, a rate-limiting enzyme in the <em>de novo</em> biosynthesis of CTP, has been shown to assemble into filamentous structures known as cytoophidium. First identified in 2010 by three independent research groups, cytoophidia are evolutionarily conserved across diverse organisms, including bacteria, archaea, yeast, mammals, and plants, suggesting a fundamental biological function. Given the well-established advantages of <em>Drosophila melanogaste</em>r as a genetic model, this organism provides a powerful system for investigating the physiological roles of cytoophidia. This review synthesizes current findings on CTPS cytoophidia in <em>Drosophila</em>, with a particular focus on their spatiotemporal distribution in tissues and their regulatory roles in three key biological processes: intestinal homeostasis, lipid metabolism, and reproductive physiology. Furthermore, we discuss the challenges and future directions in cytoophidia research, offering insights into their broader implications in cellular metabolism and physiology.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114536"},"PeriodicalIF":3.3,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143686232","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}

引用次数: 0

The mutual effects of stearoyl-CoA desaturase and cancer-associated fibroblasts: A focus on cancer biology

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-22 DOI: 10.1016/j.yexcr.2025.114508

Suleiman Ibrahim Mohammad , Asokan Vasudevan , Ahmad Hussein alzewmel , Safia Obaidur Rab , Suhas Ballal , Rishiv Kalia , J. Bethanney Janney , Subhashree Ray , Kamal Kant Joshi , Hatif Abdulrazaq Yasin

{"title":"The mutual effects of stearoyl-CoA desaturase and cancer-associated fibroblasts: A focus on cancer biology","authors":"Suleiman Ibrahim Mohammad , Asokan Vasudevan , Ahmad Hussein alzewmel , Safia Obaidur Rab , Suhas Ballal , Rishiv Kalia , J. Bethanney Janney , Subhashree Ray , Kamal Kant Joshi , Hatif Abdulrazaq Yasin","doi":"10.1016/j.yexcr.2025.114508","DOIUrl":"10.1016/j.yexcr.2025.114508","url":null,"abstract":"<div><div>The tumor microenvironment (TME) 's primary constituents that promote cancer development are cancer-associated fibroblasts (CAFs). Metabolic remodeling has been shown to control CAF activity, particularly aberrant lipid metabolism. SCD1 can be thought of as the primary enzyme controlling the fluidity of lipid bilayers by gradually converting saturated fatty acids into monounsaturated fatty acids. Furthermore, its crucial function in the onset and spread of cancer is well acknowledged. Even with the increasing amount of research on changes in lipid metabolism, this problem remains a relatively understudied aspect of cancer research. Blocking several fatty acid synthesis-related enzymes highly expressed in cancerous cells inhibits cell division and encourages apoptosis. This is the situation with SCD1, whose overexpression has been linked to several changed tumors and cells. Both genetic and pharmacological silencing of SCD1 in cancer cells prevents glucose-mediated lipogenesis and tumor cell growth. However, its role in CAFs, hence, cancer biology, has been less studied. This study aimed to review the role of SCD1 in CAF biology, shedding light on their function in cancer cell biology.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114508"},"PeriodicalIF":3.3,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691512","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}

引用次数: 0

Oxytocin receptor enhances adipocyte browning and energy metabolism in mice

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-21 DOI: 10.1016/j.yexcr.2025.114534

Xinyue Bao , Mingjun San , Shuilian Wang , Yanli Zhuo , Ziying Liu , Yaowu Zheng , Dan Li

{"title":"Oxytocin receptor enhances adipocyte browning and energy metabolism in mice","authors":"Xinyue Bao , Mingjun San , Shuilian Wang , Yanli Zhuo , Ziying Liu , Yaowu Zheng , Dan Li","doi":"10.1016/j.yexcr.2025.114534","DOIUrl":"10.1016/j.yexcr.2025.114534","url":null,"abstract":"<div><div>Obesity is characterized by abnormal adipose tissue development and disrupted energy metabolism, involving multiple factors. Oxytocin receptor (OXTR) influences social behaviors, mammary gland development and reproduction. In this study, a transgenic mouse model with universal OXTR overexpression under the β-actin promoter (<sup>++</sup><em>Oxtr</em>) was employed. Both <sup>++</sup><em>Oxtr</em> males and females exhibited a lean phenotype with reduced fat accumulation, despite unchanged food consumption. OXTR overexpression enhanced energy expenditure, adaptive thermogenesis and glucose tolerance. Morphologically, OXTR overexpression induced adipose tissue browning, marked by increased cell density and smaller adipocytes. Gene expression analysis revealed elevated levels of Brown Adipose Tissue (BAT) markers, fatty acid transport proteins and glucose transporters in adipose tissues. High OXTR ameliorated high-fat diet (HFD)-induced obesity with improvement of metabolic parameters. Mechanistically, OXTR overexpression led to an activation of PPAR signaling, increased energy expenditure, reduced fat deposition and promoted weight loss. These findings identify OXTR as a critical regulator of energy metabolism and thermogenesis. The ability of OXTR to enhance adaptive thermogenesis and energy metabolism suggests it may serve as a novel therapeutic target for metabolic disorders.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114534"},"PeriodicalIF":3.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143686656","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}

引用次数: 0

Calcium sensing receptor stimulates breast cancer cell migration and invasion via protein kinase C ζ

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-20 DOI: 10.1016/j.yexcr.2025.114523

Safir Ullah Khan , Rodolfo Daniel Cervantes-Villagrana , Jorge Eduardo del Río-Robles , Janik Adriana Tomás-Morales , Yazmin Torres-Santos , José Vázquez-Prado , Guadalupe Reyes-Cruz

{"title":"Calcium sensing receptor stimulates breast cancer cell migration and invasion via protein kinase C ζ","authors":"Safir Ullah Khan , Rodolfo Daniel Cervantes-Villagrana , Jorge Eduardo del Río-Robles , Janik Adriana Tomás-Morales , Yazmin Torres-Santos , José Vázquez-Prado , Guadalupe Reyes-Cruz","doi":"10.1016/j.yexcr.2025.114523","DOIUrl":"10.1016/j.yexcr.2025.114523","url":null,"abstract":"<div><div>Calcium-sensing receptor (CaSR), a G protein-coupled receptor, is overexpressed in certain breast cancer tumors where it drives cell migration and secretion of chemotactic agonists, likely contributing to metastatic dissemination. Since CaSR activates breast cancer cell migration via the Gβγ-PI3K-mTORC2/Rac-1 pathway, we hypothesized that PKCζ and perhaps other protein kinase C (PKC) isoforms, known as mTORC2-regulated effectors, are involved in migratory and invasive signaling elicited by CaSR. We analyzed the effect of PKC inhibitors and siRNAs which pointed to PKCζ as effector of CaSR in cell migration and invasion. In breast cancer phosphoproteomic CPTAC datasets, we identified a group of Luminal A subtype cancer patients having active PKCζ, according to its phosphorylation status at the turn motif. In addition, various phosphorylated RacGEFs, including TRIO, ARHGEF26, DOCK1 and DOCK7, clustered as phosphoproteins with active PKCζ. We therefore introduce atypical PKCζ as an effector component of the CaSR-Gβγ-PI3K-mTORC2 pathway in the activation of the promigratory small GTPase Rac. These results support ongoing initiatives to establish critical elements of the CaSR signaling pathway as potential targets in metastatic breast cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114523"},"PeriodicalIF":3.3,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691500","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}

引用次数: 0

SNHG family lncRNAs: Key players in the breast cancer progression and immune cell's modulation

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-19 DOI: 10.1016/j.yexcr.2025.114531

Mohamed J. Saadh , Junainah Abd Hamid , H. Malathi , Syeda Wajida Kazmi , Thabit Moath Omar , Ashish Sharma , M Ravi Kumar , Tushar Aggarwal , Fadhil Feez Sead

{"title":"SNHG family lncRNAs: Key players in the breast cancer progression and immune cell's modulation","authors":"Mohamed J. Saadh , Junainah Abd Hamid , H. Malathi , Syeda Wajida Kazmi , Thabit Moath Omar , Ashish Sharma , M Ravi Kumar , Tushar Aggarwal , Fadhil Feez Sead","doi":"10.1016/j.yexcr.2025.114531","DOIUrl":"10.1016/j.yexcr.2025.114531","url":null,"abstract":"<div><div>Breast cancer, a highly prevalent form of cancer worldwide, has observed a steady increase in its prevalence over the past few decades. This rise can be attributed to the complex nature of the disease, characterized by its heterogeneity, ability to metastasize, and resistance to various treatment. In the field of cancer research, long non-coding RNAs (lncRNAs) are of special interest, which play an important role in the development and progression of various tumors, including breast cancer. LncRNAs affect the tumor microenvironment by attracting diverse immunosuppressive factors and controlling the differentiation of immune cells, often referred to as myeloid and lymphoid cells, which contributes to immune escape of tumor cells. Among the lncRNA families, the small nucleolar RNA host gene (SNHG) family has been found to be dysregulated in breast cancer. These SNHGs have been implicated in crucial cellular processes such as cell proliferation, invasion, migration, resistance to therapies, apoptosis, as well as immune cell regulation and differentiation. Consequently, they have great potential as diagnostic and prognostic biomarkers as well as potential therapeutic targets for breast cancer. In this comprehensive review, we aim to summarize the recent advances in the study of SNHGs in breast cancer pathogenesis and their role in regulating the activity of immune cells in the tumor microenvironment through affecting SNHGs/miRNA/mRNA pathways, with the aim of providing new insights into the treatment of breast cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114531"},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673453","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}

引用次数: 0

FSP1 regulates ferroptosis and mitochondrial function during mouse oocyte maturation

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-03-18 DOI: 10.1016/j.yexcr.2025.114524

Hongzhen Ruan , Huifen Xiang , Yajing Liu , Peiwen Wang , Liuliu Dong , Yunxia Cao , Dan Liang , Zhiming Ding

{"title":"FSP1 regulates ferroptosis and mitochondrial function during mouse oocyte maturation","authors":"Hongzhen Ruan , Huifen Xiang , Yajing Liu , Peiwen Wang , Liuliu Dong , Yunxia Cao , Dan Liang , Zhiming Ding","doi":"10.1016/j.yexcr.2025.114524","DOIUrl":"10.1016/j.yexcr.2025.114524","url":null,"abstract":"<div><div>Oocyte quality plays a fundamental role in fertilization and embryonic development. Emerging evidence indicates that ferroptosis may impair oocyte quality. Ferroptosis suppressor protein 1 (FSP1), a known ferroptosis inhibitor, has an uncharacterized function in regulating oocyte quality during meiotic maturation. This study identified FSP1 expression across all stages of meiotic maturation with localization to the cytoplasm of mouse oocytes. Aged mice exhibited a marked reduction in FSP1 expression within the ovaries and oocytes. Pharmacological inhibition of FSP1 disrupted germinal vesicle breakdown and polar body emission, leading to spindle defects and chromosome misalignment. Additionally, FSP1 inhibition persistently activated the spindle assembly checkpoint, resulting in meiotic arrest. At the mechanistic level, inhibition of FSP1 led to an increase in intracellular Fe<sup>2+</sup> levels, enhanced dihydroethidium fluorescence, excessive accumulation of reactive oxygen species, and intensified lipid peroxidation. Disruptions in ferroptosis-associated gene expression further indicated that oocytes underwent ferroptosis. Moreover, mitochondrial dysfunction was evident following FSP1 inhibition, as reflected by aberrant mitochondrial distribution, diminished ATP production, and an elevated mitochondrial membrane potential. Collectively, these results establish FSP1 as a key regulator of oocyte meiotic maturation by modulating iron homeostasis and mitochondrial function, while its inhibition triggers ferroptosis-dependent meiotic failure.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114524"},"PeriodicalIF":3.3,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669524","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}

引用次数: 0