Li Yong-Wu, Bai Lin, Dai Lyu-Xia, He Xu, Zhou Xian-Ping
Experiment Teaching Center of Clinical Medicine, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan 610500, China.
Chin Med J (Engl). 2016 Feb 20;129(4):405-9. doi: 10.4103/0366-6999.176066.
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.
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).
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).
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.
肺癌已成为许多地区的主要死因。致癌作用是由基因和染色体变化的逐步积累引起的。本研究的目的是调查人肺腺癌细胞系OM中的染色体和基因改变。
我们使用吉姆萨显带和多重荧光原位杂交技术，聚焦于人肺腺癌细胞系OM，分析其染色体改变。此外，通过比较基因组杂交（CGH）确定特定染色体区域的增减情况，并通过聚合酶链反应（PCR）检测癌症相关基因的扩增情况。
我们在除X染色体和19号染色体外的所有染色体上发现了大量染色体数目改变。10号染色体最常参与易位，有六种不同的染色体间易位。CGH显示3q25.3 - 28、5p13、12q22 - 23.24染色体区域有增益，而3p25 - 26、6p25、6q26 - 27、7q34 - 36、8p22 - 23、9p21 - 24、10q25 - 26.3、12p13.31 - 13.33和17p13.1 - 13.3有缺失。PCR显示基因膜金属内肽酶（MME）、蔗糖酶 - 异麦芽糖酶（SI）、丁酰胆碱酯酶（BCHE）和激肽原（KNG）有扩增。
人肺腺癌细胞系OM表现出多种复杂的核型，10号染色体频繁参与染色体易位，这可能在肿瘤发生中起关键作用。我们推测癌基因可能位于3q25.3 - 28、5p13、12q22 - 23.24，而抑癌基因可能存在于3p25 - 26、6p25、6q26 - 27、7q34 - 36、8p22 - 23、9p21 - 24、10q25 - 26.3、12p13.31 - 13.33和17p13.1 - 13.3。此外，至少四个基因（MME、SI、BCHE和KNG）可能与人肺腺癌细胞系OM有关。
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