Ohmura H, Tahara H, Suzuki M, Ide T, Shimizu M, Yoshida M A, Tahara E, Shay J W, Barrett J C, Oshimura M
Department of Molecular and Cell Genetics, School of Life Sciences, Faculty of Medicine, Tottori University.
Jpn J Cancer Res. 1995 Oct;86(10):899-904. doi: 10.1111/j.1349-7006.1995.tb02998.x.
Telomeres, at the end of chromosomes, shorten with each cell division, resulting in cellular senescence. Tumor cells, unlike normal somatic cells, express a telomerase that maintains the telomere length. Deletion of a gene(s) on chromosome 3 is common in human renal cell carcinoma (RCC) and reintroduction of a normal chromosome 3 into an RCC immortal cell line restored the program of cellular senescence. The loss of indefinite growth potential was associated with the loss of telomerase activity and shortening of telomeres in the RCC cells with a normal chromosome 3. However, microcell hybrids that escaped from senescence and microcell hybrids with an introduced chromosome 7 or 11 maintained telomere lengths and telomerase activity similar to those of the parental RCC23. Thus, restoration of the cellular senescence program by chromosome 3 is associated with repression of telomerase function in RCC cells.
端粒位于染色体末端，随着细胞每次分裂而缩短，导致细胞衰老。与正常体细胞不同，肿瘤细胞表达一种维持端粒长度的端粒酶。3号染色体上一个或多个基因的缺失在人类肾细胞癌（RCC）中很常见，将一条正常的3号染色体重新导入RCC永生细胞系可恢复细胞衰老程序。在具有正常3号染色体的RCC细胞中，无限生长潜能的丧失与端粒酶活性的丧失以及端粒缩短有关。然而，逃脱衰老的微细胞杂种以及导入了7号或11号染色体的微细胞杂种维持了与亲本RCC23相似的端粒长度和端粒酶活性。因此，3号染色体恢复细胞衰老程序与RCC细胞中端粒酶功能的抑制有关。
