Nonrandom chromosomal imbalances in human ovarian surface epithelial cells immortalized by HPV16-E6E7 viral oncogenes
Nonrandom chromosomal imbalances in human ovarian surface epithelial cells immortalized by HPV16-E6E7 viral oncogenes
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DOI:
10.1016/s0165-4608(01)00473-3
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发表时间:
2001-10-15
影响因子:
--
通讯作者:
Wong, YC
中科院分区:
文献类型:
--
作者:
Tsao, SW;Wong, N;Wong, YC
We had previously immortalized human ovarian surface epithelial (HOSE) cells using HPV16E6E7 ORFs. In order to identify crucial genetic events involved during cell immortalization, the genomic profile of immortalization of five HOSE cell lines was analyzed by comparative genomic hybridization. Our results showed that chromosomal imbalance was common in HOSE cells after immortalization. The common chromosomal imbalances identified in immortal HOSE cells are: +19q13.1 (5/5 lines), -13q12 similar to qter (4/5 lines), +5q15 similar to q33 (3/5 lines), +20q11.2 similar to q13.2 (3/5 lines) and -22q11.2 similar to qter (315 lines). Other chromosomal imbalances, which were detected in two of the five immortal HOSE cell lines, included gains on chromosome 1 and 11q12 similar to q13, and losses on 2p, 4q, 8p, 10p and 11q14 similar to qter. The chromosomal imbalances observed in HOSE cells before immortalization include -8pter similar to p11.2, -11q23 similar to qter, -13q12 similar to qter and +19 which may represent early genetic events during cell immortalization. The genomic profile was examined in one HOSE cell line (HOSE 6-3) at various stages of immortalization. The genomic profiles of HOSE 6-3 cells after crisis were largely stable. A few additional chromosomal imbalances were detected in the immortalized HOSE cells after an extensive culture period including +11pter similar to q23, -15q23 similar to qter, and +17q12 similar to qter. Identification of nonrandom chromosomal imbalance in immortalized HOSE cells may facilitate the identification of specific chromosomes harboring genes involved in the immortalization of human ovarian surface epithelial cells. (C) 2001 Elsevier Science Inc. All rights reserved.