5-Bromodeoxyuridine induces senescence-like phenomena in mammalian cells regardless of cell type or species.
5-Bromodeoxyuridine was found to induce flat and enlarged cell shape, characteristics of senescent cells, and senescence-associated beta-galactosidase in mammalian cells regardless of cell type or species. In immortal human cells, fibronectin, collagenase I, and p21(wafl/sdi-1) mRNAs were immediately and very strongly induced, and the mortality marker mortalin changed to the mortal type from the immortal type. Human cell lines lacking functional p21(wafl/sdi-1), p16(ink4a), or p53 behaved similarly. The protein levels of p16(ink4a) and p53 did not change uniformly, while the level of p21(wafl/sdi-1) was increased by varying degrees in positive cell lines. Telomerase activity was suppressed in positive cell lines, but accelerated telomere shortening was not observed in tumor cell lines. These results suggest that 5-bromodeoxyuridine activates a common senescence pathway present in both mortal and immortal mammalian cells.
Michishita
E
E
Kihara Institute for Biological Research and Graduate School of Integrated Science, Yokohama City University, Totsuka-ku, Yokohama, 244-0813, Japan.
Nakabayashi
K
K
Suzuki
T
T
Kaul
S C
SC
Ogino
H
H
Fujii
M
M
Mitsui
Y
Y
Ayusawa
D
D
D000375:Aging / Q000187:drug effects*; D000818:Animals; D015415:Biomarkers; D001973:Bromodeoxyuridine / Q000494:pharmacology*; D002453:Cell Cycle; D002460:Cell Line; D004591:Electrophoresis, Polyacrylamide Gel; D006801:Humans; D051379:Mice; D012150:Polymorphism, Restriction Fragment Length; D016615:Telomere; D014407:Tumor Cells, Cultured
D015415:Biomarkers; D001973:Bromodeoxyuridine