Research
Print page Print page
Switch language
Rigshospitalet - a part of Copenhagen University Hospital
Published

p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC

Research output: Contribution to journalJournal articleResearchpeer-review

DOI

  1. Programming of adipose tissue miR-483-3p and GDF-3 expression by maternal diet in type 2 diabetes

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. The current epidemic of HPV-associated oropharyngeal cancer: An 18-year Danish population-based study with 2,169 patients

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Tumor miRNA expression profile is related to vestibular schwannoma growth rate

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. The Number of Signaling Pathways Altered by Driver Mutations in Chronic Lymphocytic Leukemia Impacts Disease Outcome

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Chromothripsis and DNA Repair Disorders

    Research output: Contribution to journalReviewResearchpeer-review

  5. Fine-mapping of 150 breast cancer risk regions identifies 191 likely target genes

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations
Aberrant oncogene activation induces cellular senescence, an irreversible growth arrest that acts as a barrier against tumorigenesis. To identify microRNAs (miRNAs) involved in oncogene-induced senescence, we examined the expression of miRNAs in primary human TIG3 fibroblasts after constitutive activation of B-RAF. Among the regulated miRNAs, both miR-34a and miR-146a were strongly induced during senescence. Although members of the miR-34 family are known to be transcriptionally regulated by p53, we find that miR-34a is regulated independently of p53 during oncogene-induced senescence. Instead, upregulation of miR-34a is mediated by the ETS family transcription factor, ELK1. During senescence, miR-34a targets the important proto-oncogene MYC and our data suggest that miR-34a thereby coordinately controls a set of cell cycle regulators. Hence, in addition to its integration in the p53 pathway, we show that alternative cancer-related pathways regulate miR-34a, emphasising its significance as a tumour suppressor.
Original languageEnglish
JournalCell Death and Differentiation
Volume17
Issue number2
Pages (from-to)236-45
Number of pages10
ISSN1350-9047
DOIs
Publication statusPublished - 1 Feb 2010

ID: 31046382