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Learn Morep53 is a transcriptional activator that induces myriad target genes. However, those p53-inducible genes most critical for tumor suppression remain elusive. Here, we identify Neat1, a ncRNA constituent of paraspeckles, as a p53 target gene induced by mouse and human p53 in different cell types and by diverse stress signals. Using fibroblasts derived from Neat1-/- mice, we examine the functional role of Neat1 in the p53 pathway. We find that Neat1 is dispensable for cell-cycle arrest and apoptosis in response to genotoxic stress, but plays a crucial role in suppressing transformation in response to oncogenic signals. To determine the effects of Neat1 deficiency on cells, we used E1A;HRasV12-expressing wild-type and Neat1-/- mouse embryonic fibroblasts (MEFs) for RNA-sequencing analysis. This analysis revealed that Neat1 deficiency impacts the regulatory networks involved in nervous system development and axon guidance programs, as well as genes of the SWI/SNF complex and components of the pancreas development network. These findings suggest that the ability of Neat1 to globally regulate gene expression, with effects on diverse transcriptional programs, provides a potential mechanism for how Neat1 acts to suppress transformation and tumor initiation. SOURCE: Stephano Spano MelloAttardi lab Stanford University
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