MiR-766 induces p53 accumulation and G2/M arrest by directly targeting MDM4

Qingqing Wang, Luke A. Selth, David F. Callen

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)
6 Downloads (Pure)


P53, a transcription factor that participates in multiple cellular functions, is considered the most important tumor suppressor. Previous evidence suggests that post-transcriptional deregulation of p53 by microRNAs contributes to tumorigenesis, tumor progression and therapeutic resistance. In the present study, we found that the microRNA miR-766 was aberrantly expressed in breast cancer, and that overexpression of miR-766 caused accumulation of wild-type p53 protein in multiple cancer cell lines. Supporting its role in the p53 signalling pathway, miR-766 decreased cell proliferation and colony formation in several cancer cell lines, and cell cycle analyses revealed that miR-766 causes G2 arrest. At a mechanistic level, we demonstrate that miR-766 enhances p53 signalling by directly targeting MDM4, an oncogene and negative regulator of p53. Analysis of clinical genomic data from multiple cancer types supports the relevance of miR-766 in p53 signalling. Collectively, our study demonstrates that miR-766 can function as a novel tumor suppressor by enhancing p53 signalling.

Original languageEnglish
Pages (from-to)29914-29924
Number of pages11
Issue number18
Publication statusPublished - 1 Jan 2017
Externally publishedYes


  • Cancer
  • Cell cycle
  • MDM4
  • MicroRNA
  • P53


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