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Cellular senescence is a crucial tumor suppressor mechanism. We discovered a CAPERα/TBX3 repressor complex required to prevent senescence in primary cells and mouse embryos. Critical, previously unknown roles for CAPERα in controlling cell proliferation are manifest in an obligatory interaction with TBX3 to regulate chromatin structure and repress transcription of  CDKN2A-p16   INK   and the RB pathway. The IncRNA  UCA1  is a direct target of CAPERα/TBX3 repression whose overexpression is sufficient to induce senescence. In proliferating cells, we found that hnRNPA1 binds and destabilizes  CDKN2A-p16   INK   mRNA whereas during senescence,  UCA1  sequesters hnRNPA1 and thus stabilizes  CDKN2A-p16   INK  . Thus CAPERα/TBX3 and  UCA1  constitute a coordinated, reinforcing mechanism to regulate both  CDKN2A-p16   INK   transcription and mRNA stability. Dissociation of the CAPERα/TBX3 co-repressor during oncogenic stress activates  UCA1 , revealing a novel mechanism for oncogene-induced senescence. Our elucidation of CAPERα and  UCA1  functions in vivo provides new insights into senescence induction, and the oncogenic and developmental properties of TBX3.

Coordinated control of senescence by lncRNA and a novel T-box3 co-repressor complex