{"title":"Circ_0060927 通过疏导 miR-331-3p 和上调 TBX2 促进结直肠癌的发展","authors":"Dian Yin, XiaoLu Zhai, Xiu Feng, Mei Hua, Jing Liu, Ying Chen","doi":"10.1016/j.prp.2024.155673","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>The dysregulation of circular RNAs (circRNAs) is closely associated with the pathogenesis of colorectal cancer (CRC). The present study aimed to elucidate the biological function and mechanism of circ_0060927 in CRC.</div></div><div><h3>Methods</h3><div>5-ethynyl-2’-deoxyuridine, Cell Counting Kit-8 (CCK-8), flow cytometry and transwell assays, as well as Xenograft tumor models were adopted for in vitro and in vivo analyses. The interaction between microRNA-331–3p (miR-331–3p) and circ_0060927 or T-box transcription factor 2 (TBX2) was verified by the dual-luciferase reporter and RNA pull-down assays.</div></div><div><h3>Results</h3><div>Circ_0060927 deficiency inhibited cell proliferation, autophagy, migration, and invasion and increased cell apoptosis and necrosis in CRC cells, as well as inhibited tumor growth <em>in vivo</em>. Circ_0060927 could bind to miR-331–3p, and circ_0060927 regulated CRC cell behaviors via sponging miR-331–3p. TBX2 was targeted by miR-331–3p, and miR-331–3p targeted TBX2 to exert the anti-cancer role in CRC cells. Mechanically, circ_0060927 regulated TBX2 expression by sequestering miR-331–3p in CRC cells.</div></div><div><h3>Conclusion</h3><div>Circ_0060927 downregulation inhibited CRC progression by regulating the miR-331–3p/TBX2 axis, which might offer a potential treatment target for CRC.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Circ_0060927 promotes colorectal cancer development by sponging miR-331-3p and upregulating TBX2\",\"authors\":\"Dian Yin, XiaoLu Zhai, Xiu Feng, Mei Hua, Jing Liu, Ying Chen\",\"doi\":\"10.1016/j.prp.2024.155673\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>The dysregulation of circular RNAs (circRNAs) is closely associated with the pathogenesis of colorectal cancer (CRC). The present study aimed to elucidate the biological function and mechanism of circ_0060927 in CRC.</div></div><div><h3>Methods</h3><div>5-ethynyl-2’-deoxyuridine, Cell Counting Kit-8 (CCK-8), flow cytometry and transwell assays, as well as Xenograft tumor models were adopted for in vitro and in vivo analyses. The interaction between microRNA-331–3p (miR-331–3p) and circ_0060927 or T-box transcription factor 2 (TBX2) was verified by the dual-luciferase reporter and RNA pull-down assays.</div></div><div><h3>Results</h3><div>Circ_0060927 deficiency inhibited cell proliferation, autophagy, migration, and invasion and increased cell apoptosis and necrosis in CRC cells, as well as inhibited tumor growth <em>in vivo</em>. Circ_0060927 could bind to miR-331–3p, and circ_0060927 regulated CRC cell behaviors via sponging miR-331–3p. TBX2 was targeted by miR-331–3p, and miR-331–3p targeted TBX2 to exert the anti-cancer role in CRC cells. Mechanically, circ_0060927 regulated TBX2 expression by sequestering miR-331–3p in CRC cells.</div></div><div><h3>Conclusion</h3><div>Circ_0060927 downregulation inhibited CRC progression by regulating the miR-331–3p/TBX2 axis, which might offer a potential treatment target for CRC.</div></div>\",\"PeriodicalId\":19916,\"journal\":{\"name\":\"Pathology, research and practice\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2024-10-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pathology, research and practice\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0344033824005843\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pathology, research and practice","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0344033824005843","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PATHOLOGY","Score":null,"Total":0}
Circ_0060927 promotes colorectal cancer development by sponging miR-331-3p and upregulating TBX2
Background
The dysregulation of circular RNAs (circRNAs) is closely associated with the pathogenesis of colorectal cancer (CRC). The present study aimed to elucidate the biological function and mechanism of circ_0060927 in CRC.
Methods
5-ethynyl-2’-deoxyuridine, Cell Counting Kit-8 (CCK-8), flow cytometry and transwell assays, as well as Xenograft tumor models were adopted for in vitro and in vivo analyses. The interaction between microRNA-331–3p (miR-331–3p) and circ_0060927 or T-box transcription factor 2 (TBX2) was verified by the dual-luciferase reporter and RNA pull-down assays.
Results
Circ_0060927 deficiency inhibited cell proliferation, autophagy, migration, and invasion and increased cell apoptosis and necrosis in CRC cells, as well as inhibited tumor growth in vivo. Circ_0060927 could bind to miR-331–3p, and circ_0060927 regulated CRC cell behaviors via sponging miR-331–3p. TBX2 was targeted by miR-331–3p, and miR-331–3p targeted TBX2 to exert the anti-cancer role in CRC cells. Mechanically, circ_0060927 regulated TBX2 expression by sequestering miR-331–3p in CRC cells.
Conclusion
Circ_0060927 downregulation inhibited CRC progression by regulating the miR-331–3p/TBX2 axis, which might offer a potential treatment target for CRC.
期刊介绍:
Pathology, Research and Practice provides accessible coverage of the most recent developments across the entire field of pathology: Reviews focus on recent progress in pathology, while Comments look at interesting current problems and at hypotheses for future developments in pathology. Original Papers present novel findings on all aspects of general, anatomic and molecular pathology. Rapid Communications inform readers on preliminary findings that may be relevant for further studies and need to be communicated quickly. Teaching Cases look at new aspects or special diagnostic problems of diseases and at case reports relevant for the pathologist''s practice.