PKCα regulates translocation of cytoplasmic pErk1/2 to nuclei in senescent cells
Lee, Yun Yeong; Kim, Hong Seok; Choi, Yong won; Ryu, Min Sook; Lim, In Kyoung
Department of Biochemistry & Molecular Biology
Cellular senescence plays a key role in the biology of aging and carcinogenesis. Hayflick and Moorhead described about replicative senescence revealing a limited proliferative capacity, and postulated cellular senescence as an in vitro manifestation of human aging (1). By employing primary cultures of human diploid fibroblast (HDF) in DMEM-high glucose, we have studied about the various phenotypes found in the process of the replicative senescence and its molecular mechanism (2, 3). In our study, the number of population doublings (PDs) of HDF was calculated by the equation; PDs=log[A/BC]/log2 (A; numbers of collected cells, B:plated cells, C; attachment efficiency), and its doubling time (DT) was counted based on the number of PDs. Young cells used in this study reveal the DT around 26 h, while DT of mid-old and old cells were 7–10 and over 14 days, respectively. We are going to discuss about the nuclear translocation of pErk1/2 sequestered in the cytoplasm of senescent cells in response to TPA treatment along with induction of cell proliferation. Our study may imply a molecular mechanism of the higher incidence of cancer development in the aged than the young people via nuclear translocation of pErk1/2 in senescent cells after exposed to a tumor promoter.
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