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高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究
BACKGROUND AND OBJECTIVE: Invasion and metastasis is one of malignant phenotype of lung cancer and the important cause of the death of lung cancer patients. The aim of this study is to explore the methylation profile difference in different metastatic potential cell lines. METHODS: To compare the DN...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
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中国肺癌杂志编辑部
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000560/ https://www.ncbi.nlm.nih.gov/pubmed/20704814 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.08.02 |
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collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Invasion and metastasis is one of malignant phenotype of lung cancer and the important cause of the death of lung cancer patients. The aim of this study is to explore the methylation profile difference in different metastatic potential cell lines. METHODS: To compare the DNA methylation profile of two large cell lung cancer cell lines with different metastatic potential by MeIP chip hybridization, hypermethylated and hypomethylated genes of L9981 cell lines were analyzed online in NIH-DAVID, KEGG and MILANO webside. RESULTS: Compared with NL9980 cell line, 735 genes are hypermethylated in L9981, including 656 known genes and 79 unknown genes; 809 gene are hypermethylated in L9981, including 698 known genes and 111 unknown genes; the different genes are involved in cell process, signal transduction, cell communication, cell adhesion, cell motility, and angiogenesis. CONCLUSION: Hypermethylation of suppressor genes and negative regulator of signal transduction and hopomethylation of oncogene and cell adhesion molecules (CAMs) in L9981 may promote metastasis of tumor cells. |
format | Online Article Text |
id | pubmed-6000560 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
spelling | pubmed-60005602018-07-06 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Invasion and metastasis is one of malignant phenotype of lung cancer and the important cause of the death of lung cancer patients. The aim of this study is to explore the methylation profile difference in different metastatic potential cell lines. METHODS: To compare the DNA methylation profile of two large cell lung cancer cell lines with different metastatic potential by MeIP chip hybridization, hypermethylated and hypomethylated genes of L9981 cell lines were analyzed online in NIH-DAVID, KEGG and MILANO webside. RESULTS: Compared with NL9980 cell line, 735 genes are hypermethylated in L9981, including 656 known genes and 79 unknown genes; 809 gene are hypermethylated in L9981, including 698 known genes and 111 unknown genes; the different genes are involved in cell process, signal transduction, cell communication, cell adhesion, cell motility, and angiogenesis. CONCLUSION: Hypermethylation of suppressor genes and negative regulator of signal transduction and hopomethylation of oncogene and cell adhesion molecules (CAMs) in L9981 may promote metastasis of tumor cells. 中国肺癌杂志编辑部 2010-08-20 /pmc/articles/PMC6000560/ /pubmed/20704814 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.08.02 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 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 |
title | 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 |
title_full | 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 |
title_fullStr | 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 |
title_full_unstemmed | 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 |
title_short | 高低转移大细胞肺癌细胞株L9981和NL9980间甲基化差异基因的初步研究 |
title_sort | 高低转移大细胞肺癌细胞株l9981和nl9980间甲基化差异基因的初步研究 |
topic | 基础研究 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000560/ https://www.ncbi.nlm.nih.gov/pubmed/20704814 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.08.02 |
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