{"title":"lncRNA LINC00265通过TATA-Box结合蛋白相关因子1调控肺癌细胞增殖的作用","authors":"Qian Chen, Jinhong Xu, Aiming Hu, Ying Zhang","doi":"10.1134/s2079086424020038","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Lung cancer is a serious public health problem because of high mortality and poor prognosis. A growing body of evidence suggests that long non-coding RNAs (lncRNAs) play a crucial role in cancer. This study aims to investigate lncRNA LINC00265 in NSCLC. The purpose of this study was to investigate the role and molecular mechanism of LINC00265 NSCLC. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of LINC00265. CCK-8 assay was used to analyze cell proliferation. Transwell assay, Scratch trial respectively were used to detect cell invasion and migration ability. The interaction between LINC00265 and TAF1 was predicted by bioinformatics tool starBasev 2.0 and verified by Dual-Luciferase reporter assay. The protein level of EMT was quantified by Western blot. LINC00265 was upregulated in lung cancer tissues. LINC00265 knockdown restrained the viability, proliferation, and migration of lung cancer cells and promoted cell apoptosis, while transfected LINC00265 reversed these effects. Mechanistically, LINC00265 might interact with TAF1 to regulated cell biological processes. This study identified LINC00265 as a tumor activator in NSCLC. LINC00265 participated in the progression of lung cancer through TAF1 regulatory axis at least in part. Our study supplied a promising target for the treatment of lung cancer.</p>","PeriodicalId":9047,"journal":{"name":"Biology Bulletin Reviews","volume":"105 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Role of lncRNA LINC00265 in Regulating Proliferation of Lung Cancer Cells via TATA-Box Binding Protein Associated Factor 1\",\"authors\":\"Qian Chen, Jinhong Xu, Aiming Hu, Ying Zhang\",\"doi\":\"10.1134/s2079086424020038\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<h3 data-test=\\\"abstract-sub-heading\\\">Abstract</h3><p>Lung cancer is a serious public health problem because of high mortality and poor prognosis. A growing body of evidence suggests that long non-coding RNAs (lncRNAs) play a crucial role in cancer. This study aims to investigate lncRNA LINC00265 in NSCLC. The purpose of this study was to investigate the role and molecular mechanism of LINC00265 NSCLC. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of LINC00265. CCK-8 assay was used to analyze cell proliferation. Transwell assay, Scratch trial respectively were used to detect cell invasion and migration ability. The interaction between LINC00265 and TAF1 was predicted by bioinformatics tool starBasev 2.0 and verified by Dual-Luciferase reporter assay. The protein level of EMT was quantified by Western blot. LINC00265 was upregulated in lung cancer tissues. LINC00265 knockdown restrained the viability, proliferation, and migration of lung cancer cells and promoted cell apoptosis, while transfected LINC00265 reversed these effects. Mechanistically, LINC00265 might interact with TAF1 to regulated cell biological processes. This study identified LINC00265 as a tumor activator in NSCLC. LINC00265 participated in the progression of lung cancer through TAF1 regulatory axis at least in part. Our study supplied a promising target for the treatment of lung cancer.</p>\",\"PeriodicalId\":9047,\"journal\":{\"name\":\"Biology Bulletin Reviews\",\"volume\":\"105 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-02-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biology Bulletin Reviews\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1134/s2079086424020038\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biology Bulletin Reviews","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1134/s2079086424020038","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Role of lncRNA LINC00265 in Regulating Proliferation of Lung Cancer Cells via TATA-Box Binding Protein Associated Factor 1
Abstract
Lung cancer is a serious public health problem because of high mortality and poor prognosis. A growing body of evidence suggests that long non-coding RNAs (lncRNAs) play a crucial role in cancer. This study aims to investigate lncRNA LINC00265 in NSCLC. The purpose of this study was to investigate the role and molecular mechanism of LINC00265 NSCLC. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of LINC00265. CCK-8 assay was used to analyze cell proliferation. Transwell assay, Scratch trial respectively were used to detect cell invasion and migration ability. The interaction between LINC00265 and TAF1 was predicted by bioinformatics tool starBasev 2.0 and verified by Dual-Luciferase reporter assay. The protein level of EMT was quantified by Western blot. LINC00265 was upregulated in lung cancer tissues. LINC00265 knockdown restrained the viability, proliferation, and migration of lung cancer cells and promoted cell apoptosis, while transfected LINC00265 reversed these effects. Mechanistically, LINC00265 might interact with TAF1 to regulated cell biological processes. This study identified LINC00265 as a tumor activator in NSCLC. LINC00265 participated in the progression of lung cancer through TAF1 regulatory axis at least in part. Our study supplied a promising target for the treatment of lung cancer.