{"title":"AC125611.3通过募集DKC1稳定CTNNB1来促进癌症的进展。","authors":"Hanqing Tang , Yuyu Dou , Yiliang Meng , Qinglan Lu , Lingling Liang","doi":"10.1016/j.ajg.2022.10.013","DOIUrl":null,"url":null,"abstract":"<div><h3>Background and study aims</h3><p><span>Previous studies have suggested that lncRNAs impact cancer progression. The lncRNA AC125611.3 (also referred to as RP11-161H23.5) is highly expressed in </span>colon cancer but rarely studied; understanding its regulation may provide novel insights on treating colon cancer.</p></div><div><h3>Materials and methods</h3><p>qRT-PCR was performed to quantify RNAs. CCK-8 and EdU assays were performed to assess cell proliferation<span><span><span><span>. Western blot analysis was used to detect levels of proteins related to cell </span>apoptosis and </span>EMT<span>. Wound healing assay and Transwell invasion assay were conducted to evaluate cell migratory and invasive capabilities, respectively. Luciferase reporter assay, </span></span>RIP assay, and pull-down assay were used to verify RNA-RNA and RNA-protein interactions.</span></p></div><div><h3>Results</h3><p><span>AC125611.3 was highly overexpressed in colon cancer cells. AC125611.3 depletion curbed cell proliferative, invasive, migratory, and EMT processes while enhancing apoptosis. Furthermore, AC125611.3 activated the Wnt signaling pathway in colon cancer cells by regulating catenin beta-1 (CTNNB1). Moreover, AC125611.3 recruited </span>dyskeratosis congenita 1 (DKC1) to stabilize CTNNB1.</p></div><div><h3>Conclusion</h3><p>AC125611.3 recruits DKC1 to stabilize CTNNB1 and activate Wnt signaling, thereby promoting the progression of colon cancer.</p></div>","PeriodicalId":48674,"journal":{"name":"Arab Journal of Gastroenterology","volume":null,"pages":null},"PeriodicalIF":1.1000,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"AC125611.3 promotes the progression of colon cancer by recruiting DKC1 to stabilize CTNNB1\",\"authors\":\"Hanqing Tang , Yuyu Dou , Yiliang Meng , Qinglan Lu , Lingling Liang\",\"doi\":\"10.1016/j.ajg.2022.10.013\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background and study aims</h3><p><span>Previous studies have suggested that lncRNAs impact cancer progression. The lncRNA AC125611.3 (also referred to as RP11-161H23.5) is highly expressed in </span>colon cancer but rarely studied; understanding its regulation may provide novel insights on treating colon cancer.</p></div><div><h3>Materials and methods</h3><p>qRT-PCR was performed to quantify RNAs. CCK-8 and EdU assays were performed to assess cell proliferation<span><span><span><span>. Western blot analysis was used to detect levels of proteins related to cell </span>apoptosis and </span>EMT<span>. Wound healing assay and Transwell invasion assay were conducted to evaluate cell migratory and invasive capabilities, respectively. Luciferase reporter assay, </span></span>RIP assay, and pull-down assay were used to verify RNA-RNA and RNA-protein interactions.</span></p></div><div><h3>Results</h3><p><span>AC125611.3 was highly overexpressed in colon cancer cells. AC125611.3 depletion curbed cell proliferative, invasive, migratory, and EMT processes while enhancing apoptosis. Furthermore, AC125611.3 activated the Wnt signaling pathway in colon cancer cells by regulating catenin beta-1 (CTNNB1). Moreover, AC125611.3 recruited </span>dyskeratosis congenita 1 (DKC1) to stabilize CTNNB1.</p></div><div><h3>Conclusion</h3><p>AC125611.3 recruits DKC1 to stabilize CTNNB1 and activate Wnt signaling, thereby promoting the progression of colon cancer.</p></div>\",\"PeriodicalId\":48674,\"journal\":{\"name\":\"Arab Journal of Gastroenterology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2023-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Arab Journal of Gastroenterology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1687197922000910\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arab Journal of Gastroenterology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1687197922000910","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
AC125611.3 promotes the progression of colon cancer by recruiting DKC1 to stabilize CTNNB1
Background and study aims
Previous studies have suggested that lncRNAs impact cancer progression. The lncRNA AC125611.3 (also referred to as RP11-161H23.5) is highly expressed in colon cancer but rarely studied; understanding its regulation may provide novel insights on treating colon cancer.
Materials and methods
qRT-PCR was performed to quantify RNAs. CCK-8 and EdU assays were performed to assess cell proliferation. Western blot analysis was used to detect levels of proteins related to cell apoptosis and EMT. Wound healing assay and Transwell invasion assay were conducted to evaluate cell migratory and invasive capabilities, respectively. Luciferase reporter assay, RIP assay, and pull-down assay were used to verify RNA-RNA and RNA-protein interactions.
Results
AC125611.3 was highly overexpressed in colon cancer cells. AC125611.3 depletion curbed cell proliferative, invasive, migratory, and EMT processes while enhancing apoptosis. Furthermore, AC125611.3 activated the Wnt signaling pathway in colon cancer cells by regulating catenin beta-1 (CTNNB1). Moreover, AC125611.3 recruited dyskeratosis congenita 1 (DKC1) to stabilize CTNNB1.
Conclusion
AC125611.3 recruits DKC1 to stabilize CTNNB1 and activate Wnt signaling, thereby promoting the progression of colon cancer.
期刊介绍:
Arab Journal of Gastroenterology (AJG) publishes different studies related to the digestive system. It aims to be the foremost scientific peer reviewed journal encompassing diverse studies related to the digestive system and its disorders, and serving the Pan-Arab and wider community working on gastrointestinal disorders.