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Long noncoding RNAs (lncRNAs) have emerged as a major regulator of cell physiology, but many of which have no known function. CDKN1A/p21 is an important inhibitor of the cell-cycle, regulator of the DNA damage response and effector of the tumor suppressor p53, playing a crucial role in tumor development and prevention. In order to identify a regulator for tumor progression, we performed an siRNA screen of human lncRNAs required for cell proliferation, and identified a novel lncRNA,  APTR , that acts in  trans  to repress the  CDKN1A/p21  promoter independent of  p53  to promote cell proliferation.  APTR  associates with the promoter of  CDKN1A/p21  and this association requires a complementary- Alu  sequence encoded in  APTR . A different module of  APTR  associates with and recruits the Polycomb repressive complex 2 (PRC2) to epigenetically repress the  p21  promoter. A decrease in  APTR  is necessary for the induction of p21 after heat stress and DNA damage by doxorubicin, and the levels of  APTR  and  p21  are anti-correlated in human glioblastomas. Our data identify a new regulator of the cell-cycle inhibitor  CDKN1A/p21  that acts as a proliferative factor in cancer cell lines and in glioblastomas and demonstrate that  Alu  elements present in lncRNAs can contribute to targeting regulatory lncRNAs to promoters.

A New lncRNA, APTR, Associates with and Represses the CDKN1A/p21 Promoter by Recruiting Polycomb Proteins