Cell and Bioscience最新文献

{"title":"The lncRNA MIR181A1HG in extracellular vesicles derived from highly metastatic colorectal cancer cells promotes liver metastasis by remodeling the extracellular matrix and recruiting myeloid-derived suppressor cells.","authors":"Yichao Gu, Yushuai Mi, Yifan Cao, Kuan Yu, Zihao Zhang, Peng Lian, Dawei Li, Jing Qin, Senlin Zhao","doi":"10.1186/s13578-025-01365-2","DOIUrl":"10.1186/s13578-025-01365-2","url":null,"abstract":"<p><strong>Background: </strong>Colorectal liver metastasis (CRLM) is the main cause of death in colorectal cancer (CRC) patients worldwide. In the initial stage of metastasis, primary tumors provide the necessary conditions for metastasis by shaping the local microenvironment of the target organ, forming \"premetastatic niches\" (PMNs), and extracellular vesicles (EVs) play important roles in shaping PMNs. Therefore, investigating the EVs involved in the regulation of PMNs and their mechanism is highly valuable for the further understanding of CRLM.</p><p><strong>Methods: </strong>Transmission electron microscopy and differential ultracentrifugation were used to verify the existence of exosomes. In vivo and in vitro assays were used to identify the roles of MIR181A1HG in EVs in CRLM. RNA pull-down and dual-luciferase reporter assays were used to clarify the mechanism by which MIR181A1HG in EVs regulated the crosstalk between CRC cells and hepatic stellate cells (HSCs).</p><p><strong>Results: </strong>We demonstrated that the lncRNA MIR181A1HG was progressively upregulated in tissues, serum EVs from healthy normal controls to CRC and paired liver metastatic groups. Additionally, we verified that HNRNPA2B1 mediated the packaging of MIR181A1HG into CRC cell-derived EVs, which in turn functioned as a ceRNA by sponging miR373-3p to activate HSCs via the TGFβRII/Smad2/3 signaling pathway. Furthermore, activated HSCs could secrete the chemokine CXCL12 to promote CRLM by remodeling the extracellular matrix and recruiting myeloid-derived suppressor cells in the liver, which resulted in liver metastasis.</p><p><strong>Conclusions: </strong>MIR181A1HG in EVs from highly metastatic CRC cells promoted CRLM by activating HSCs to form PMNs in the liver, which contributes to the further understanding of the mechanism of CRLM and provides potential predictive markers for CRLM.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"23"},"PeriodicalIF":6.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KAT8 catalyzes the acetylation of SEPP1 at lysine 247/249 and modulates the activity of CD8⁺ T cells via LRP8 to promote anti-tumor immunity in pancreatic cancer.","authors":"Zhongfei Zhu, Gang Nie, Xiaobo Peng, Xianbao Zhan, Dan Ding","doi":"10.1186/s13578-025-01356-3","DOIUrl":"10.1186/s13578-025-01356-3","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic cancer (PC) remains one of the most lethal malignancies with unfavorable prognosis globally. Bioinformatics analysis predicted that SEPP1 was low expressed in PC and related to tumor immune microenvironment, but its biological function was still unclear.</p><p><strong>Methods: </strong>PC xenograft and liver metastasis mouse models, as well as PC cell-MDSCs co-culture system, were established for in vivo and in vitro studies, respectively. The expression and localization of key molecules were detected by qRT-PCR, western blot, immunohistochemistry and immunofluorescence. Flow cytometry was employed to assess the abundance of immune cells and cell apoptosis. The interactions among KAT8, SEPP1 and LRP8 were detected by co-IP. Cell viability, migration and invasion were monitored by CCK-8 and transwell assays.</p><p><strong>Results: </strong>SEPP1 was downregulated in pancreatic tumors, and it was positively correlated with the abundance of CD8⁺ T cells. In vivo overexpression of SEPP1 impaired PC tumor growth and liver metastasis via modulating the abundance of CD8⁺ T cell and MDSCs. KAT8 upregulated SEPP1 transcription and protein level via catalyzing the acetylation at K247/249 on SEPP1, and SEPP1 impaired MDSCs survival via its receptor LRP8, thus regulating CD8⁺ T cell-mediated immune responses in PC. In vivo studies further revealed that SEPP1 recombinant protein enhanced the efficacy of anti-PD-1 therapy in PC xenograft mouse model.</p><p><strong>Conclusion: </strong>KAT8 catalyzed the acetylation of SEPP1 at K247/249 and modulated the activity of CD8⁺ T cells via LRP8 to promote anti-tumor immunity in PC.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"24"},"PeriodicalIF":6.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enpp1 ameliorates MAFLD by regulating hepatocyte lipid metabolism through the AMPK/PPARα signaling pathway.","authors":"Xiaohui Liu, Shuai Chen, Xing Liu, Xianxian Wu, Xiaoliang Jiang, Yuhan Li, Zhiwei Yang","doi":"10.1186/s13578-025-01364-3","DOIUrl":"10.1186/s13578-025-01364-3","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the leading chronic liver disease globally, and there are no approved pharmacotherapies to treat this disease. Ectonucleotide pyrophosphatase/phosphodiesterase 1 (Enpp1) has been found to be related to insulin resistance and lipid accumulation. However, the role and mechanism of Enpp1 in the development of MAFLD remain unknown.</p><p><strong>Results: </strong>Here we discovered that Enpp1 is lowly expressed in the liver of MAFLD patients by clinical investigation. Knocking out Enpp1 in the liver of mice aggravated obesity, insulin resistance and hepatic steatosis, and these effects were reversed by liver-specific Enpp1 overexpression. Through transcriptomic data mining and experimental validation, we demonstrated that Enpp1 deficiency inhibited the expression of AMPK (energy receptor) and PPARα (nuclear transcription factor for lipid metabolism), thereby promoting the transcription of lipid synthesis factors and mediating the progression of MAFLD. Mechanistically, Enpp1 enhanced the activity of AMPK by increasing the AMP-to-ATP ratio, which in turn raised PPARα levels and promoted the transcription of its downstream lipid metabolism factors. Pharmacological inhibition of AMPK activity abolished the promoting effect of Enpp1 on PPARα protein expression.</p><p><strong>Conclusions: </strong>This study indicate that Enpp1 can effectively ameliorate MAFLD through effects on AMPK/PPARα signaling pathway-mediated lipid metabolism, revealing the significance of Enpp1 as a promising therapeutic target against MAFLD.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"22"},"PeriodicalIF":6.1,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircRNA Itm2b induces oxidative stress via the interaction with Sirt1-Nox4 to aggravate sleep disturbances after traumatic brain injury.","authors":"Jiayuanyuan Fu, Mengran Du, Biying Wu, Chenrui Wu, Xin Li, Weilin Tan, Xuekang Huang, Ziyu Zhu, Jie Zhang, Zheng Bu Liao","doi":"10.1186/s13578-025-01353-6","DOIUrl":"10.1186/s13578-025-01353-6","url":null,"abstract":"<p><p>Sleep disorders (SD) are common sequelae following traumatic brain injury (TBI) and may be linked to mitochondrial oxidative stress dysregulation after TBI. Increasing evidence showed that circRNAs play crucial roles in nervous system diseases. However, the involvement of circRNAs in sleep disturbances after TBI is not characterized. In this study, differentially expressed circRNAs were identified by RNA sequencing. Sleep quality in TBI patients was assessed through sleep scales and electroencephalograms. Further experiments were conducted to investigate the role of circItm2b. We found that circItm2b was elevated and involved sleep disorder in TBI patients. Over-expression of circItm2b might aggravate sleep disturbances in mice after TBI. Mechanically, circItm2b regulates Nox4 expression through binding Sirt1, which influences mitochondrial oxidative stress-caused circadian protein losses. Moreover, the knockdown of circItm2b attenuated mitochondrial oxidative stress-induced circadian proteins losses via circItm2b/Sirt1/Nox4 axis after TBI, which might suggest that circItm2b may serve as a prognostic marker for improving sleep disorders and represent a promising therapeutic target for TBI-related sleep disturbances.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"21"},"PeriodicalIF":6.1,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-pathway targeted therapy of MASH-HCC using miR-22.","authors":"Ying Hu, Tahereh Setayesh, Dongguang Wei, Trenton Testerman, Yutong Ji, Yu-Jui Yvonne Wan","doi":"10.1186/s13578-025-01352-7","DOIUrl":"10.1186/s13578-025-01352-7","url":null,"abstract":"<p><strong>Background: </strong>The treatment options for hepatocellular carcinoma (HCC) are limited, and there is no effective drug that can improve long-term survival rates. Complicated cocktails consisting of multiple medications with toxicities are frequently used to treat cancer. The current study addresses these challenges.</p><p><strong>Methods: </strong>The study uses metabolic dysfunction-associated steatohepatitis (MASH)-HCC and HCC mouse models established by transfecting the livers using myr-AKT1, NRasV12, and Sleeping Beauty transposase. AAV8-miR-22 was delivered to MASH-HCC and HCC to study its preventive and therapeutic effects. Spatial transcriptomic profiling revealed the signaling pathways affected by miR-22 according to histological locations.</p><p><strong>Results: </strong>miR-22 treatment effectively treated MASH-HCC and HCC. Treating mice with miR-22 before tumor initiation prevented oncogenesis. The promising anti-cancer effects were revealed by reduced tumor load, fibrosis, and splenomegaly, extending the survival time. miR-22 treatment generated anti-tumor immunity. The favorable treatment outcomes were accompanied by a reduction in dendritic cells, T and B cells, and plasma cells, which were expanded inside the tumors of MASH-HCC. In all animal trials, miR-22 improved metabolism and reduced glycolysis inside the tumors. Moreover, miR-22 profoundly inhibited extracellular matrix (ECM) and targeted MET, PDGF, tyrosine kinase signaling, and IGF pathways inside the tumors. Furthermore, the roles of miR-22 in blocking collagen formation and cross-assembly of collagen fibrils could be due to miR-22's effects in inhibiting Rho GTPase pathways, revealed at the tumor margin.</p><p><strong>Conclusion: </strong>miR-22 generates anti-HCC effects by targeting many critical pathways in liver carcinogenesis in cancer and tumorigenic niches, potentially revolutionizing HCC treatment.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"20"},"PeriodicalIF":6.1,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide association study of the fatty liver index in the Taiwanese population reveals shared and population-specific genetic risk factors across ethnicities.","authors":"Pei Pei Lau, Chun-Yu Wei, Min-Rou Lin, Wan-Hsuan Chou, Yu-Jui Yvonne Wan, Wei-Chiao Chang","doi":"10.1186/s13578-025-01346-5","DOIUrl":"10.1186/s13578-025-01346-5","url":null,"abstract":"<p><strong>Background and objectives: </strong>Although the incidence of fatty liver disease (FLD) is increasing worldwide, the genetic basis of this disease is not fully understood. This study uses the fatty liver index (FLI) to identify and compare genetic variants associated with FLD in Taiwanese and European populations.</p><p><strong>Results: </strong>In this study, a total of 145,356 Taiwan Biobank participants were included in the discovery analysis. Subjects with elevated FLI were found to have a significantly greater risk of developing FLD, as confirmed by imaging data (OR: 4.43; 95% CI: 3.88-5.06). Through genome-wide association studies (GWAS), we identified 6 variants previously associated with nonalcoholic fatty liver disease (NAFLD) and validated 50 shared risk variants located in ZPR1 and FTO between the Taiwanese and European populations. Conditional analysis of 423 significant variants from FLI-defined FLD further revealed 16 independent variants within 14 genes. Pathway analysis of GWAS significant genes revealed that lipid metabolism and the peroxisome proliferator-activated receptor (PPAR) signaling pathway are causes of hepatic fat accumulation.</p><p><strong>Conclusion: </strong>This study identified six independent NAFLD-associated variants in GCKR, LPL, TRIB1AL, and FTO and emphasized ZPR1 and FTO as shared risk genes for FLI-defined FLD in both Taiwanese and European populations. These findings support the utility of the FLI for FLD prediction, provide new genetic insights, and reveal the common genetic pathways of FLD across two ethnic groups. This research offers a valuable framework for advancing personalized medicine and therapeutic strategies for FLD.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"19"},"PeriodicalIF":6.1,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11807309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TOPBP1 as a potential predictive biomarker for enhanced combinatorial efficacy of olaparib and AZD6738 in PDAC.","authors":"Xiao-Mei Tang, Min-Min Shi, Jia-Cheng Wang, Yi-Jin Gu, Yu-Ting Dai, Qin-Xin Yang, Jia Liu, Ling-Jie Ren, Xin-Yun Liu, Chun Yang, Fang-Fang Ma, Ji-Bing Liu, Hong Yu, Da Fu, Yun-Feng Wang","doi":"10.1186/s13578-025-01350-9","DOIUrl":"10.1186/s13578-025-01350-9","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive and often lethal malignancy, requiring the development of enhanced therapeutic approaches. The DNA damage response (DDR) pathway is frequently altered during PDAC development, leading to an increased occurrence of DNA damage. DNA topoisomerase II-binding protein 1 (TOPBP1) plays a supportive role in regulating the DDR pathway, and its overexpression has been linked to the tumorigenesis of various cancers. This study investigated the biological role of TOPBP1 in PDAC pathogenesis and evaluated its clinical relevance in guiding treatment regimens. We examined the relationship between TOPBP1 expression, DDR pathway modulation, and therapeutic response in PDAC cell lines, primary cells, and subcutaneous mouse models. We found that elevated TOPBP1 expression was positively correlated with increased histologic grade and reduced patient survival in PDAC. TOPBP1 knockdown increased the sensitivity of PDAC cells to olaparib treatment and improved therapeutic efficacy in both PDAC cell lines and subcutaneous mouse models. Combination treatment with olaparib and AZD6738 effectively induced P53-dependent apoptosis via inhibiting the ATR pathway and enhancing signaling through the ATM pathway, which significantly reduced the viability of pancreatic cell lines. Notably, this combination therapy was more effective in PDAC cell lines exhibiting high TOPBP1 expression, indicating that TOPBP1 may serve as a useful predictive biomarker. In conclusion, TOPBP1 is a potential marker for optimizing the olaparib and AZD6738 combination therapy in PDAC. This study highlights the clinical significance of TOPBP1 in the treatment of PDAC and emphasizes the potential implications for a broader population of patients.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"17"},"PeriodicalIF":6.1,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143371410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of characteristics and immune responses between paired human nasal and bronchial epithelial organoids.","authors":"Lu Zhu, Wenhao Yang, Jiaxin Luo, Danli Lu, Yanan Hu, Rui Zhang, Yan Li, Li Qiu, Zelian Chen, Lina Chen, Hanmin Liu","doi":"10.1186/s13578-024-01342-1","DOIUrl":"10.1186/s13578-024-01342-1","url":null,"abstract":"<p><strong>Background: </strong>The nasal epithelium, as part of a continuous and integrated airway epithelium, provides a more accessible sample source than the bronchial epithelium. However, the similarities and differences in gene expression patterns and immune responses between these two sites have not been extensively studied.</p><p><strong>Results: </strong>Four lines of matched nasal and bronchial airway epithelial cells obtained from the four patients were embedded in Matrigel and cultured in thechemically defined medium to generate patient-derived nasal organoids (NO) and bronchial organoids (BO). Histologic examination of nasal organoid tissue revealed high similarity and a reduced ciliary beat frequency compared to bronchial organoid tissue. Whole exome sequencing revealed that over 99% of single nucleotides were shared between the NO and matched BO and there was a 95% overlap in their RNA transcriptomes. RNA sequencing analysis of differentially expressed genes indicated a significant reduction in the immune response in NO. RSV infection revealed more productive replication in NO, with a downregulated immune pathway identified by RNA sequencing analysis and upregulated levels of pro-inflammatory cytokines in culture supernatants in NO compared to BO.</p><p><strong>Conclusions: </strong>NO and BO serve as robust in vitro models, faithfully recapitulating the biological characteristics of upper respiratory epithelial cells. The different regions of respiratory epithelial cells exhibit distinct immune responses, underscoring their complementary roles in exploring airway immune mechanisms and disease pathophysiology.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"18"},"PeriodicalIF":6.1,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143371401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive landscape and oncogenic role of extrachromosomal circular DNA in malignant biliary strictures.","authors":"Zhuo Cheng, Xuanmei Luo, Wenzheng Liu, Xiaofang Lu, Hong Chang, Yingchun Wang, Wei Zheng, Xiue Yan, Yonghui Huang","doi":"10.1186/s13578-025-01361-6","DOIUrl":"10.1186/s13578-025-01361-6","url":null,"abstract":"<p><strong>Background: </strong>Extrachromosomal circular DNA (eccDNA) is crucial for carcinogenesis and bile has direct contact with malignant biliary strictures, yet eccDNA features in bile and its function in malignant biliary strictures remain underexplored.</p><p><strong>Results: </strong>We observed the widespread presence of eccDNA in bile and systematically profiled the landscape of bile cell-free eccDNA (bcf-eccDNA). For functional exploration, a simple and efficient workflow was designed to synthesize large eccDNA particularly containing multiple regions. Compared with the noncancer group, bcf-eccDNAs in the cancer group had different origins and larger sizes with six characteristic peaks. These peaks were also identified in the validation cohort (100%). There were more bcf-eccDNA carrying LINC00598 or CELF2 in malignant biliary strictures, showing potential diagnostic performance in training and validation cohorts (all AUCs > 0.9). Bcf-eccDNAs carried cancer-related mutations, which could guide treatment. EccDNA carrying miR-106a/363 cluster or miR-374b/421 cluster were proven to regulate cancer gene expression, accelerate tumor proliferation, and inhibit tumor apoptosis.</p><p><strong>Conclusions: </strong>This study profiles a comprehensive bcf-eccDNA landscape in patients with biliary strictures and offers valuable insights into eccDNA's role in bile liquid biopsy and carcinogenesis.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"16"},"PeriodicalIF":6.1,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11804034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143371404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plectin, a novel regulator in migration, invasion and adhesion of ovarian cancer.","authors":"Lanning Bai, Xueqian Qian, Hui Zhang, Yi Yuan, Xiaodong Cui, Min Cheng, Yangyang Han","doi":"10.1186/s13578-025-01349-2","DOIUrl":"10.1186/s13578-025-01349-2","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer (OC) is one of the most prevalent gynecologic malignancies and exhibites the highest fatality rate among all gynecologic malignancies. The absence of an early diagnostic biomarker and therapeutic target contributes to an overall 5-year survival rate ranging from 30 to 50%. Plectin (PLEC), a 500 kDa scaffolding protein, has gained prominence in recent years due to its pivotal role in various cellular biological functions such as cell morphology, migration and adhesion, while the accurate role of PLEC in OC remains elusive.</p><p><strong>Results: </strong>In this study, our findings demonstrate that PLEC exerts a positive influence on the progression of OC, encompassing cellular proliferation, migration, invasion, and adhesion both in vitro and in vivo.</p><p><strong>Conclusions: </strong>The results providing new insights for the diagnosis and treatment in OC.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"15 1","pages":"15"},"PeriodicalIF":6.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11804098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}