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人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研

BACKGROUND AND OBJECTIVE: The expression of TSLC1 is downregulated or abrogated in many kinds of tumors, and its downregulation is highly associated with DNA hypermethlyation. The aim of this study is to explore the relationship between TSLC1 silencing and DNA methylation of its promoter region in l...

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Formato: Online Artículo Texto
Lenguaje:English
Publicado: 中国肺癌杂志编辑部 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000693/
https://www.ncbi.nlm.nih.gov/pubmed/20677643
http://dx.doi.org/10.3779/j.issn.1009-3419.2010.05.16
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collection PubMed
description BACKGROUND AND OBJECTIVE: The expression of TSLC1 is downregulated or abrogated in many kinds of tumors, and its downregulation is highly associated with DNA hypermethlyation. The aim of this study is to explore the relationship between TSLC1 silencing and DNA methylation of its promoter region in lung cancer cells. METHODS: We detected the expression patern of TSLC1 in human normal lung tissue and three lung cancer cell lines (A549, NCI-H446 and Calu-3) by semi-quantitative RT-PCR and Real-time PCR. Ten we detected the status of DNA methylation in TSLC1 promoter region with bisulfte sequencing in above normal lung tissue and lung cancer cell lines. Afer treatment of above cell lines with the inhibitor of DNA methyltransferase 5-Aza-2-deoxycytidine (5-Aza-dC), we detected the expression change of TSLC1 by Real-time PCR before and afer the treatment of 5-Aza-dC. RESULTS: There was no methylation in TSLC1 promoter region in normal lung tissue and A549 cell line in which TSLC1 expressed; while there was DNA hypermethylation in TSLC1 promoter region in NCI-H446 and Calu-3 cell lines in which TSLC1 was abrogated, also the expression of TSLC1 in NCI-H446 and Calu-3 cell lines could be restored afer treatment of 5-Aza-dC. CONCLUSION: The silencing of TSLC1 in lung cancer cells is due to the hypermethylation of its promoter region.
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spelling pubmed-60006932018-07-06 人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: The expression of TSLC1 is downregulated or abrogated in many kinds of tumors, and its downregulation is highly associated with DNA hypermethlyation. The aim of this study is to explore the relationship between TSLC1 silencing and DNA methylation of its promoter region in lung cancer cells. METHODS: We detected the expression patern of TSLC1 in human normal lung tissue and three lung cancer cell lines (A549, NCI-H446 and Calu-3) by semi-quantitative RT-PCR and Real-time PCR. Ten we detected the status of DNA methylation in TSLC1 promoter region with bisulfte sequencing in above normal lung tissue and lung cancer cell lines. Afer treatment of above cell lines with the inhibitor of DNA methyltransferase 5-Aza-2-deoxycytidine (5-Aza-dC), we detected the expression change of TSLC1 by Real-time PCR before and afer the treatment of 5-Aza-dC. RESULTS: There was no methylation in TSLC1 promoter region in normal lung tissue and A549 cell line in which TSLC1 expressed; while there was DNA hypermethylation in TSLC1 promoter region in NCI-H446 and Calu-3 cell lines in which TSLC1 was abrogated, also the expression of TSLC1 in NCI-H446 and Calu-3 cell lines could be restored afer treatment of 5-Aza-dC. CONCLUSION: The silencing of TSLC1 in lung cancer cells is due to the hypermethylation of its promoter region. 中国肺癌杂志编辑部 2010-05-20 /pmc/articles/PMC6000693/ /pubmed/20677643 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.05.16 Text en 版权所有©《中国肺癌杂志》编辑部2010 https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/
spellingShingle 基础研究
人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研
title 人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研
title_full 人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研
title_fullStr 人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研
title_full_unstemmed 人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研
title_short 人肺癌细胞中TSLC1基因表达缺失与DNA甲基化的相关性研
title_sort 人肺癌细胞中tslc1基因表达缺失与dna甲基化的相关性研
topic 基础研究
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000693/
https://www.ncbi.nlm.nih.gov/pubmed/20677643
http://dx.doi.org/10.3779/j.issn.1009-3419.2010.05.16
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