{"title":"LncRNA SLC16A1-AS1通过靶向miR-515-5p调控MAP3K9表达参与结直肠癌的发生和进展。","authors":"Wanxing Xu, Suzhen Bi, Meichun Xing","doi":"10.62347/ABOI7514","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of long non-coding RNA (lncRNA) SLC16A1-AS1 in the initiation and progression of colorectal cancer (CRC).</p><p><strong>Methods: </strong>Cell viability was tested using Cell Counting Kit-8 (CCK-8). Cell invasion and migration were evaluated using Transwell assays, and apoptosis was determined by flow cytometry. Gene expression was tested by qRT-PCR or Western blot. The targeting relationship between miR-515-5p and MAP3K9 was verified using bioinformatics tools, RNA immunoprecipitation (RIP) experiments, and dual-luciferase reporter assays.</p><p><strong>Results: </strong>Both lncRNA SLC16A1-AS1 and MAP3K9 were upregulated in CRC cells, while miR-515-5p expression was downregulated. Overexpression of miR-515-5p and silencing of lncRNA SLC16A1-AS1 inhibited CRC cell proliferation, suppressed cell invasion and migration, and promoted cell apoptosis. The targeting relationship between lncRNA SLC16A1-AS1 and miR-515-5p, as well as between MAP3K9 and miR-515-5p, were confirmed by bioinformatics, RIP assays, and luciferase reporter assays.</p><p><strong>Conclusion: </strong>lncRNA SLC16A1-AS1 contributes to the initiation and progression of CRC by modulating miR-515-5p to regulate MAP3K9 expression, providing potential insights for CRC treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"14 11","pages":"5539-5550"},"PeriodicalIF":3.6000,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626282/pdf/","citationCount":"0","resultStr":"{\"title\":\"LncRNA SLC16A1-AS1 participates in the initiation and progression of colorectal cancer by regulating MAP3K9 expression through targeting miR-515-5p.\",\"authors\":\"Wanxing Xu, Suzhen Bi, Meichun Xing\",\"doi\":\"10.62347/ABOI7514\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To investigate the role of long non-coding RNA (lncRNA) SLC16A1-AS1 in the initiation and progression of colorectal cancer (CRC).</p><p><strong>Methods: </strong>Cell viability was tested using Cell Counting Kit-8 (CCK-8). Cell invasion and migration were evaluated using Transwell assays, and apoptosis was determined by flow cytometry. Gene expression was tested by qRT-PCR or Western blot. The targeting relationship between miR-515-5p and MAP3K9 was verified using bioinformatics tools, RNA immunoprecipitation (RIP) experiments, and dual-luciferase reporter assays.</p><p><strong>Results: </strong>Both lncRNA SLC16A1-AS1 and MAP3K9 were upregulated in CRC cells, while miR-515-5p expression was downregulated. Overexpression of miR-515-5p and silencing of lncRNA SLC16A1-AS1 inhibited CRC cell proliferation, suppressed cell invasion and migration, and promoted cell apoptosis. The targeting relationship between lncRNA SLC16A1-AS1 and miR-515-5p, as well as between MAP3K9 and miR-515-5p, were confirmed by bioinformatics, RIP assays, and luciferase reporter assays.</p><p><strong>Conclusion: </strong>lncRNA SLC16A1-AS1 contributes to the initiation and progression of CRC by modulating miR-515-5p to regulate MAP3K9 expression, providing potential insights for CRC treatment.</p>\",\"PeriodicalId\":7437,\"journal\":{\"name\":\"American journal of cancer research\",\"volume\":\"14 11\",\"pages\":\"5539-5550\"},\"PeriodicalIF\":3.6000,\"publicationDate\":\"2024-11-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626282/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of cancer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/ABOI7514\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/ABOI7514","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
LncRNA SLC16A1-AS1 participates in the initiation and progression of colorectal cancer by regulating MAP3K9 expression through targeting miR-515-5p.
Objective: To investigate the role of long non-coding RNA (lncRNA) SLC16A1-AS1 in the initiation and progression of colorectal cancer (CRC).
Methods: Cell viability was tested using Cell Counting Kit-8 (CCK-8). Cell invasion and migration were evaluated using Transwell assays, and apoptosis was determined by flow cytometry. Gene expression was tested by qRT-PCR or Western blot. The targeting relationship between miR-515-5p and MAP3K9 was verified using bioinformatics tools, RNA immunoprecipitation (RIP) experiments, and dual-luciferase reporter assays.
Results: Both lncRNA SLC16A1-AS1 and MAP3K9 were upregulated in CRC cells, while miR-515-5p expression was downregulated. Overexpression of miR-515-5p and silencing of lncRNA SLC16A1-AS1 inhibited CRC cell proliferation, suppressed cell invasion and migration, and promoted cell apoptosis. The targeting relationship between lncRNA SLC16A1-AS1 and miR-515-5p, as well as between MAP3K9 and miR-515-5p, were confirmed by bioinformatics, RIP assays, and luciferase reporter assays.
Conclusion: lncRNA SLC16A1-AS1 contributes to the initiation and progression of CRC by modulating miR-515-5p to regulate MAP3K9 expression, providing potential insights for CRC treatment.
期刊介绍：
The American Journal of Cancer Research (AJCR) (ISSN 2156-6976), is an independent open access, online only journal to facilitate rapid dissemination of novel discoveries in basic science and treatment of cancer. It was founded by a group of scientists for cancer research and clinical academic oncologists from around the world, who are devoted to the promotion and advancement of our understanding of the cancer and its treatment. The scope of AJCR is intended to encompass that of multi-disciplinary researchers from any scientific discipline where the primary focus of the research is to increase and integrate knowledge about etiology and molecular mechanisms of carcinogenesis with the ultimate aim of advancing the cure and prevention of this increasingly devastating disease. To achieve these aims AJCR will publish review articles, original articles and new techniques in cancer research and therapy. It will also publish hypothesis, case reports and letter to the editor. Unlike most other open access online journals, AJCR will keep most of the traditional features of paper print that we are all familiar with, such as continuous volume, issue numbers, as well as continuous page numbers to retain our comfortable familiarity towards an academic journal.
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