Abstract
To explore the genetic mechanism of replicative senescence, we identified and cloned a Cellular Senescence-Inhibited Gene/ribosomal L1 domain containing 1 (CSIG/RSL1D1) through suppressive subtractive hybridization. CSIG expression is high in earlypassaged human diploid fibroblast cells but decreased during senescence. Our results demonstrated that CSIG inhibited the senescence progression and mediated the apoptosis signaling pathway under ultraviolet (UV) irradiation. Moreover, emerging evidences have indicated that CSIG is involved in other processes including cell cycle regulation and tumor development. This is a brief overview to introduce the studies on the function and molecular mechanism of CSIG
Highlights
Replicative senescence, a cellular self-protection mechanism to prevent tumor development, contributes to the generation of age-related disorders [1,2,3]
By analysis of dog osteosarcoma samples, Selvarajah et al found that CSIG was related to tumor cells survival and associated with cell proliferation and cancer metastasis [11], and CSIG may act as a new therapeutic target
We recently discovered that the downstream genes modulated by CSIG are mainly implicated in the processes of cell cycle, apoptosis, transcriptional control, bone formation and cell adhesion [14], which further provides the molecular basis for CSIG to participate in these biological processes
Summary
Replicative senescence, a cellular self-protection mechanism to prevent tumor development, contributes to the generation of age-related disorders [1,2,3]. CSIG expression is high in early-passaged human diploid fibroblast cells but decreased during senescence [4,5]. The experiments in vivo and in vitro both indicated that CSIG is associated with cellular senescence and participates in organismal aging [4].
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