Open AccessRestoration of the Cellular Senescence Program and Repression of Telomerase by Human Chromosome 3
Author(s) -
Ohmura Hiroshi,
Tahara Hidetoshi,
Suzuki Mikio,
Ide Toshinori,
Shimizu Motoyuki,
Yoshida Mitsuaki A.,
Tahara Eiichi,
Shay Jerry W.,
Barrett J. Carl,
Oshimura Mitsuo
Publication year - 1995
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1995.tb02998.x
Subject(s) - telomerase , telomere , senescence , biology , somatic cell , chromosome , microbiology and biotechnology , telomerase reverse transcriptase , microcell , cell division , genetics , cell , gene , computer science , operating system
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.