Abstract
Cellular senescence is a stress response and a permanent state of cell cycle arrest of normal cell division. SENEBLOC is involved in both oncogenic and replicative senescence and has been identified as a c-Myc responsive lncRNA involved in senescence. SENEBLOC acts to restrains p21-mediated senescence. Mouse double minute 2 (MDM2) regulates p53, controls its transcriptional activity and protein stability. Cyclin-dependent kinase (CDK) inhibitor p21 promotes cell cycle arrest in response to a variety of stimuli and it can be induced by both p53-dependent and p53-independent mechanisms. SENEBLOC is shown to drive both p53-dependent and p53-independent mechanisms. SENEBLOC acts as a scaffold to promote p53 turnover. It decreases p21 transactivation and promotes p53 and MDM2 association. p53-independent regulation of p21 by SENEBLOC occurs via regulatory effects on HDAC5. Rapamycin promotes SENEBLOC transcription through effects on E2F1. In this review, I focus on the importance of the newly identified LncRNA SENEBLOC
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