{"title":"Hsa_circ_0000423通过竞争性吸附介导 CCND1 表达的 miR-369-3p 来促进结直肠癌 EMT 和免疫逃逸。","authors":"TianFu Huang, KaiHai Jiang, LinTao Li, GuangSheng Li, YuSheng Cao, XuSen Huang","doi":"10.1007/s12672-024-01501-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>This investigation evaluated the mechanism of hsa_circ_0000423 in colorectal cancer (CRC).</p><p><strong>Methods: </strong>The hsa_circ_0000423 gene was identified by bioinformatics analyses of GEO circRNA microarrays, and its expression in CRC was investigated. Based on this, in vitro experiments were conducted. Assays with dual luciferase reporter and RIP were conducted to detect interactions between hsa_circ_0000423, miR-369-3p and CCND1. Cell proliferation was measured by MTT and colony formation assay assays, apoptosis was detected by flow cytometry, migration and invasion were detected by Transwell, and expression of EMT-related proteins was detected by Western Blot. SW480 cells and T cells were co-cultured to assess immune escape.</p><p><strong>Results: </strong>hsa_circ_0000423 and CCND1 were elevated in CRC while miR-369-3p was downregulated Silencing hsa_circ_0000423 resulted in reduced CCND1 expression by upregulating miR-369-3p. Overexpressing CCND1 or down-regulating miR-369-3p both interrupted the anti-tumor role of silencing hsa_circ_0000423 on CRC cells.</p><p><strong>Conclusion: </strong>Hsa_circ_0000423 promotes CCND1 expression through competitive binding of miR-369-3p and promotes CRC cell development and immune escape.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550305/pdf/","citationCount":"0","resultStr":"{\"title\":\"Hsa_circ_0000423 promotes colorectal cancer EMT and immune escape by competitive adsorption of miR-369-3p mediating CCND1 expression.\",\"authors\":\"TianFu Huang, KaiHai Jiang, LinTao Li, GuangSheng Li, YuSheng Cao, XuSen Huang\",\"doi\":\"10.1007/s12672-024-01501-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>This investigation evaluated the mechanism of hsa_circ_0000423 in colorectal cancer (CRC).</p><p><strong>Methods: </strong>The hsa_circ_0000423 gene was identified by bioinformatics analyses of GEO circRNA microarrays, and its expression in CRC was investigated. Based on this, in vitro experiments were conducted. Assays with dual luciferase reporter and RIP were conducted to detect interactions between hsa_circ_0000423, miR-369-3p and CCND1. Cell proliferation was measured by MTT and colony formation assay assays, apoptosis was detected by flow cytometry, migration and invasion were detected by Transwell, and expression of EMT-related proteins was detected by Western Blot. SW480 cells and T cells were co-cultured to assess immune escape.</p><p><strong>Results: </strong>hsa_circ_0000423 and CCND1 were elevated in CRC while miR-369-3p was downregulated Silencing hsa_circ_0000423 resulted in reduced CCND1 expression by upregulating miR-369-3p. Overexpressing CCND1 or down-regulating miR-369-3p both interrupted the anti-tumor role of silencing hsa_circ_0000423 on CRC cells.</p><p><strong>Conclusion: </strong>Hsa_circ_0000423 promotes CCND1 expression through competitive binding of miR-369-3p and promotes CRC cell development and immune escape.</p>\",\"PeriodicalId\":11148,\"journal\":{\"name\":\"Discover. Oncology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2024-11-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550305/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Discover. Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12672-024-01501-3\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Discover. Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12672-024-01501-3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Hsa_circ_0000423 promotes colorectal cancer EMT and immune escape by competitive adsorption of miR-369-3p mediating CCND1 expression.
Background: This investigation evaluated the mechanism of hsa_circ_0000423 in colorectal cancer (CRC).
Methods: The hsa_circ_0000423 gene was identified by bioinformatics analyses of GEO circRNA microarrays, and its expression in CRC was investigated. Based on this, in vitro experiments were conducted. Assays with dual luciferase reporter and RIP were conducted to detect interactions between hsa_circ_0000423, miR-369-3p and CCND1. Cell proliferation was measured by MTT and colony formation assay assays, apoptosis was detected by flow cytometry, migration and invasion were detected by Transwell, and expression of EMT-related proteins was detected by Western Blot. SW480 cells and T cells were co-cultured to assess immune escape.
Results: hsa_circ_0000423 and CCND1 were elevated in CRC while miR-369-3p was downregulated Silencing hsa_circ_0000423 resulted in reduced CCND1 expression by upregulating miR-369-3p. Overexpressing CCND1 or down-regulating miR-369-3p both interrupted the anti-tumor role of silencing hsa_circ_0000423 on CRC cells.
Conclusion: Hsa_circ_0000423 promotes CCND1 expression through competitive binding of miR-369-3p and promotes CRC cell development and immune escape.
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