| General information | Literature | Expression | Regulation | Mutation | Interaction |
|
Basic Information |
|
|---|---|
Gene ID | 406967 |
Name | MIR192 |
Synonymous | MIRN192|miR-192|miRNA192;microRNA 192;MIR192;microRNA 192 |
Definition | hsa-mir-192 |
Position | 11q13.1 |
Gene type | ncRNA |
|
Title |
Abstract |
| Coordinated regulation of cell cycle transcripts by p53-Inducible microRNAs, miR-192 and miR-215. | Cell cycle arrest in response to DNA damage is an important antitumorigenic mechanism. microRNAs (miRNAs) were recently shown to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G(1) arrest by down-regulating multiple cell cycle-related transcripts. Here we show that genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs miR-192 and miR-215. Like miR-34a, activation of miR-192/215 induces cell cycle arrest, suggesting that multiple miRNA families operate in the p53 network. Furthermore, we define a downstream gene expression signature for miR-192/215 expression, which includes a number of transcripts that regulate G(1) and G(2) checkpoints. Of these transcripts, 18 transcripts are direct targets of miR-192/215, and the observed cell cycle arrest likely results from a cooperative effect among the modulations of these genes by the miRNAs. Our results showing a role for miR-192/215 in cell proliferation combined with recent observations that these miRNAs are underexpressed in primary cancers support the idea that miR-192 and miR-215 function as tumor suppressors. |