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Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM

BACKGROUND: Lung cancer has become the leading cause of death in many regions. Carcinogenesis is caused by the stepwise accumulation of genetic and chromosomal changes. The aim of this study was to investigate the chromosome and gene alterations in the human lung adenocarcinoma cell line OM. METHODS...

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Autores principales: Li, Yong-Wu, Bai, Lin, Dai, Lyu-Xia, He, Xu, Zhou, Xian-Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4800840/
https://www.ncbi.nlm.nih.gov/pubmed/26879013
http://dx.doi.org/10.4103/0366-6999.176066
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author Li, Yong-Wu
Bai, Lin
Dai, Lyu-Xia
He, Xu
Zhou, Xian-Ping
author_facet Li, Yong-Wu
Bai, Lin
Dai, Lyu-Xia
He, Xu
Zhou, Xian-Ping
author_sort Li, Yong-Wu
collection PubMed
description BACKGROUND: Lung cancer has become the leading cause of death in many regions. Carcinogenesis is caused by the stepwise accumulation of genetic and chromosomal changes. The aim of this study was to investigate the chromosome and gene alterations in the human lung adenocarcinoma cell line OM. METHODS: We used Giemsa banding and multiplex fluorescence in situ hybridization focusing on the human lung adenocarcinoma cell line OM to analyze its chromosome alterations. In addition, the gains and losses in the specific chromosome regions were identified by comparative genomic hybridization (CGH) and the amplifications of cancer-related genes were also detected by polymerase chain reaction (PCR). RESULTS: We identified a large number of chromosomal numerical alterations on all chromosomes except chromosome X and 19. Chromosome 10 is the most frequently involved in translocations with six different interchromosomal translocations. CGH revealed the gains on chromosome regions of 3q25.3-28, 5p13, 12q22-23.24, and the losses on 3p25-26, 6p25, 6q26-27, 7q34-36, 8p22-23, 9p21-24, 10q25-26.3, 12p13.31-13.33 and 17p13.1-13.3. And PCR showed the amplification of genes: Membrane metalloendopeptidase (MME), sucrase-isomaltase (SI), butyrylcholinesterase (BCHE), and kininogen (KNG). CONCLUSIONS: The lung adenocarcinoma cell line OM exhibited multiple complex karyotypes, and chromosome 10 was frequently involved in chromosomal translocation, which may play key roles in tumorigenesis. We speculated that the oncogenes may be located at 3q25.3-28, 5p13, 12q22-23.24, while tumor suppressor genes may exist in 3p25-26, 6p25, 6q26-27, 7q34-36, 8p22-23, 9p21-24, 10q25-26.3, 12p13.31-13.33, and 17p13.1-13.3. Moreover, at least four genes (MME, SI, BCHE, and KNG) may be involved in the human lung adenocarcinoma cell line OM.
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spelling pubmed-48008402016-04-04 Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM Li, Yong-Wu Bai, Lin Dai, Lyu-Xia He, Xu Zhou, Xian-Ping Chin Med J (Engl) Original Article BACKGROUND: Lung cancer has become the leading cause of death in many regions. Carcinogenesis is caused by the stepwise accumulation of genetic and chromosomal changes. The aim of this study was to investigate the chromosome and gene alterations in the human lung adenocarcinoma cell line OM. METHODS: We used Giemsa banding and multiplex fluorescence in situ hybridization focusing on the human lung adenocarcinoma cell line OM to analyze its chromosome alterations. In addition, the gains and losses in the specific chromosome regions were identified by comparative genomic hybridization (CGH) and the amplifications of cancer-related genes were also detected by polymerase chain reaction (PCR). RESULTS: We identified a large number of chromosomal numerical alterations on all chromosomes except chromosome X and 19. Chromosome 10 is the most frequently involved in translocations with six different interchromosomal translocations. CGH revealed the gains on chromosome regions of 3q25.3-28, 5p13, 12q22-23.24, and the losses on 3p25-26, 6p25, 6q26-27, 7q34-36, 8p22-23, 9p21-24, 10q25-26.3, 12p13.31-13.33 and 17p13.1-13.3. And PCR showed the amplification of genes: Membrane metalloendopeptidase (MME), sucrase-isomaltase (SI), butyrylcholinesterase (BCHE), and kininogen (KNG). CONCLUSIONS: The lung adenocarcinoma cell line OM exhibited multiple complex karyotypes, and chromosome 10 was frequently involved in chromosomal translocation, which may play key roles in tumorigenesis. We speculated that the oncogenes may be located at 3q25.3-28, 5p13, 12q22-23.24, while tumor suppressor genes may exist in 3p25-26, 6p25, 6q26-27, 7q34-36, 8p22-23, 9p21-24, 10q25-26.3, 12p13.31-13.33, and 17p13.1-13.3. Moreover, at least four genes (MME, SI, BCHE, and KNG) may be involved in the human lung adenocarcinoma cell line OM. Medknow Publications & Media Pvt Ltd 2016-02-20 /pmc/articles/PMC4800840/ /pubmed/26879013 http://dx.doi.org/10.4103/0366-6999.176066 Text en Copyright: © 2016 Chinese Medical Journal http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Original Article
Li, Yong-Wu
Bai, Lin
Dai, Lyu-Xia
He, Xu
Zhou, Xian-Ping
Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM
title Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM
title_full Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM
title_fullStr Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM
title_full_unstemmed Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM
title_short Chromosomal and Genetic Analysis of a Human Lung Adenocarcinoma Cell Line OM
title_sort chromosomal and genetic analysis of a human lung adenocarcinoma cell line om
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4800840/
https://www.ncbi.nlm.nih.gov/pubmed/26879013
http://dx.doi.org/10.4103/0366-6999.176066
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