Haiyan Liu, Jiaming Wu, Jin Gong, Jing Zhu, Jie Liu, Xiaoqing Chen, Shaohua Qu, Jintao Chen, Zhisheng Zhou, Xulong Fan
{"title":"circash1l介导的三阴性乳腺癌肿瘤进展：PI3K/AKT通路机制","authors":"Haiyan Liu, Jiaming Wu, Jin Gong, Jing Zhu, Jie Liu, Xiaoqing Chen, Shaohua Qu, Jintao Chen, Zhisheng Zhou, Xulong Fan","doi":"10.1515/med-2025-1261","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the impact of circASH1L on subcutaneous tumor growth in nude mice with triple-negative breast cancer via the PI3K/AKT pathway.</p><p><strong>Methods: </strong>The study was conducted using bioinformatics and animal experimental verification methods. circASH1L levels in triple-negative breast cancer (TNBC) were analyzed using a dataset from the gene expression omnibus database. In the animal experiment part, nude mice were divided into shNC group, shcircASH1L-1 group, Oe-NC group, and Oe-circASH1L group. Each group was treated with corresponding circASH1L overexpression or knockdown and transplanted tumor modeling. Immunohistochemistry and western blot experiments were used to verify the effect of circASH1L on the growth of nude mouse transplanted tumors and the PI3K/AKT pathway.</p><p><strong>Results: </strong>A total of 43 circRNAs were significantly associated with TNBC, among which circASH1L was significantly highly expressed in TNBC. circASH1L-1 negatively regulates tumor volume, mass, expression rate of Ki67 cells, and PI3K/AKT pathway marker proteins.</p><p><strong>Conclusions: </strong>CircASH1L is a tumor promoter in TNBC. The expression level of circASH1L influences both the proliferation of TNBC cells and the growth of TNBC nude mice tumors by modulating the PI3K/AKT pathway.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"20 1","pages":"20251261"},"PeriodicalIF":1.6000,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413791/pdf/","citationCount":"0","resultStr":"{\"title\":\"CircASH1L-mediated tumor progression in triple-negative breast cancer: PI3K/AKT pathway mechanisms.\",\"authors\":\"Haiyan Liu, Jiaming Wu, Jin Gong, Jing Zhu, Jie Liu, Xiaoqing Chen, Shaohua Qu, Jintao Chen, Zhisheng Zhou, Xulong Fan\",\"doi\":\"10.1515/med-2025-1261\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To investigate the impact of circASH1L on subcutaneous tumor growth in nude mice with triple-negative breast cancer via the PI3K/AKT pathway.</p><p><strong>Methods: </strong>The study was conducted using bioinformatics and animal experimental verification methods. circASH1L levels in triple-negative breast cancer (TNBC) were analyzed using a dataset from the gene expression omnibus database. In the animal experiment part, nude mice were divided into shNC group, shcircASH1L-1 group, Oe-NC group, and Oe-circASH1L group. Each group was treated with corresponding circASH1L overexpression or knockdown and transplanted tumor modeling. Immunohistochemistry and western blot experiments were used to verify the effect of circASH1L on the growth of nude mouse transplanted tumors and the PI3K/AKT pathway.</p><p><strong>Results: </strong>A total of 43 circRNAs were significantly associated with TNBC, among which circASH1L was significantly highly expressed in TNBC. circASH1L-1 negatively regulates tumor volume, mass, expression rate of Ki67 cells, and PI3K/AKT pathway marker proteins.</p><p><strong>Conclusions: </strong>CircASH1L is a tumor promoter in TNBC. The expression level of circASH1L influences both the proliferation of TNBC cells and the growth of TNBC nude mice tumors by modulating the PI3K/AKT pathway.</p>\",\"PeriodicalId\":19715,\"journal\":{\"name\":\"Open Medicine\",\"volume\":\"20 1\",\"pages\":\"20251261\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-08-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12413791/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Open Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1515/med-2025-1261\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1515/med-2025-1261","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
CircASH1L-mediated tumor progression in triple-negative breast cancer: PI3K/AKT pathway mechanisms.
Objective: To investigate the impact of circASH1L on subcutaneous tumor growth in nude mice with triple-negative breast cancer via the PI3K/AKT pathway.
Methods: The study was conducted using bioinformatics and animal experimental verification methods. circASH1L levels in triple-negative breast cancer (TNBC) were analyzed using a dataset from the gene expression omnibus database. In the animal experiment part, nude mice were divided into shNC group, shcircASH1L-1 group, Oe-NC group, and Oe-circASH1L group. Each group was treated with corresponding circASH1L overexpression or knockdown and transplanted tumor modeling. Immunohistochemistry and western blot experiments were used to verify the effect of circASH1L on the growth of nude mouse transplanted tumors and the PI3K/AKT pathway.
Results: A total of 43 circRNAs were significantly associated with TNBC, among which circASH1L was significantly highly expressed in TNBC. circASH1L-1 negatively regulates tumor volume, mass, expression rate of Ki67 cells, and PI3K/AKT pathway marker proteins.
Conclusions: CircASH1L is a tumor promoter in TNBC. The expression level of circASH1L influences both the proliferation of TNBC cells and the growth of TNBC nude mice tumors by modulating the PI3K/AKT pathway.
期刊介绍：
Open Medicine is an open access journal that provides users with free, instant, and continued access to all content worldwide. The primary goal of the journal has always been a focus on maintaining the high quality of its published content. Its mission is to facilitate the exchange of ideas between medical science researchers from different countries. Papers connected to all fields of medicine and public health are welcomed. Open Medicine accepts submissions of research articles, reviews, case reports, letters to editor and book reviews.
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