{"title":"tfap2a调控的CRNDE通过RIPK3相互作用促进结肠癌进展和化疗耐药","authors":"Xin Gao, Yanming Huang, Tonghui Wei, Jingmin Xue, Filippov Iurii, Laishou Yang, Liying Wang, Hao Li, Genshen Mo, Yuze Huang, Haonan Xie, Hang Wang, Shenghan Lou, Peng Han","doi":"10.1007/s10142-025-01545-w","DOIUrl":null,"url":null,"abstract":"<div><p>Colon cancer (CC) is a common malignancy with rising incidence worldwide. Despite advances in treatment strategies, many patients still face a poor prognosis due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as important regulators of various biological processes and have been implicated in cancer progression. Among them, colorectal neoplasia differentially expressed (CRNDE) has drawn attention for its potential roles in different cancers. However, its specific functions in CC remain unclear. In this study, we identified CRNDE as highly expressed in CC, contributing to tumor progression and drug resistance. Mechanically, CRNDE is regulated by the transcription factor TFAP2A. Additionally, CRNDE inhibits pyroptosis, a form of programmed cell death, by promoting the ubiquitin-mediated degradation of RIPK3, thereby reducing the sensitivity of CC cells to 5-fluorouracil (5-FU). Our findings suggest that the TFAP2A/CRNDE/RIPK3 axis plays critical roles in colon cancer progression and chemoresistance, highlighting potential therapeutic targets for improving treatment outcomes.</p></div>","PeriodicalId":574,"journal":{"name":"Functional & Integrative Genomics","volume":"25 1","pages":""},"PeriodicalIF":3.9000,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10142-025-01545-w.pdf","citationCount":"0","resultStr":"{\"title\":\"TFAP2A-regulated CRNDE enhances colon cancer progression and chemoresistance via RIPK3 interaction\",\"authors\":\"Xin Gao, Yanming Huang, Tonghui Wei, Jingmin Xue, Filippov Iurii, Laishou Yang, Liying Wang, Hao Li, Genshen Mo, Yuze Huang, Haonan Xie, Hang Wang, Shenghan Lou, Peng Han\",\"doi\":\"10.1007/s10142-025-01545-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Colon cancer (CC) is a common malignancy with rising incidence worldwide. Despite advances in treatment strategies, many patients still face a poor prognosis due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as important regulators of various biological processes and have been implicated in cancer progression. Among them, colorectal neoplasia differentially expressed (CRNDE) has drawn attention for its potential roles in different cancers. However, its specific functions in CC remain unclear. In this study, we identified CRNDE as highly expressed in CC, contributing to tumor progression and drug resistance. Mechanically, CRNDE is regulated by the transcription factor TFAP2A. Additionally, CRNDE inhibits pyroptosis, a form of programmed cell death, by promoting the ubiquitin-mediated degradation of RIPK3, thereby reducing the sensitivity of CC cells to 5-fluorouracil (5-FU). Our findings suggest that the TFAP2A/CRNDE/RIPK3 axis plays critical roles in colon cancer progression and chemoresistance, highlighting potential therapeutic targets for improving treatment outcomes.</p></div>\",\"PeriodicalId\":574,\"journal\":{\"name\":\"Functional & Integrative Genomics\",\"volume\":\"25 1\",\"pages\":\"\"},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2025-02-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://link.springer.com/content/pdf/10.1007/s10142-025-01545-w.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Functional & Integrative Genomics\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://link.springer.com/article/10.1007/s10142-025-01545-w\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Functional & Integrative Genomics","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s10142-025-01545-w","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
TFAP2A-regulated CRNDE enhances colon cancer progression and chemoresistance via RIPK3 interaction
Colon cancer (CC) is a common malignancy with rising incidence worldwide. Despite advances in treatment strategies, many patients still face a poor prognosis due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as important regulators of various biological processes and have been implicated in cancer progression. Among them, colorectal neoplasia differentially expressed (CRNDE) has drawn attention for its potential roles in different cancers. However, its specific functions in CC remain unclear. In this study, we identified CRNDE as highly expressed in CC, contributing to tumor progression and drug resistance. Mechanically, CRNDE is regulated by the transcription factor TFAP2A. Additionally, CRNDE inhibits pyroptosis, a form of programmed cell death, by promoting the ubiquitin-mediated degradation of RIPK3, thereby reducing the sensitivity of CC cells to 5-fluorouracil (5-FU). Our findings suggest that the TFAP2A/CRNDE/RIPK3 axis plays critical roles in colon cancer progression and chemoresistance, highlighting potential therapeutic targets for improving treatment outcomes.
期刊介绍：
Functional & Integrative Genomics is devoted to large-scale studies of genomes and their functions, including systems analyses of biological processes. The journal will provide the research community an integrated platform where researchers can share, review and discuss their findings on important biological questions that will ultimately enable us to answer the fundamental question: How do genomes work?
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