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Disrupting the pairing between let-7 and Hmga2 enhances oncogenic transformation.

MicroRNAs (miRNAs) are approximately 22-nucleotide RNAs that can pair to sites within messenger RNAs to specify posttranscriptional repression of these messages. Aberrant miRNA expression can contribute to tumorigenesis, but which of the many miRNA-target relationships are relevant to this process has been unclear. Here, we report that chromosomal translocations previously associated with human tumors disrupt repression of High Mobility Group A2 (Hmga2) by let-7 miRNA. This disrupted repression promotes anchorage-independent growth, a characteristic of oncogenic transformation. Thus, losing miRNA-directed repression of an oncogene provides a mechanism for tumorigenesis, and disrupting a single miRNA-target interaction can produce an observable phenotype in mammalian cells.

Pubmed ID: 17322030


  • Mayr C
  • Hemann MT
  • Bartel DP


Science (New York, N.Y.)

Publication Data

March 16, 2007

Associated Grants

  • Agency: NIDDK NIH HHS, Id: R01 DK068348
  • Agency: NIDDK NIH HHS, Id: R01 DK068348-01
  • Agency: NIDDK NIH HHS, Id: R01 DK068348-02
  • Agency: NIDDK NIH HHS, Id: R01 DK068348-03

Mesh Terms

  • 3' Untranslated Regions
  • Animals
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Transformation, Neoplastic
  • Gene Expression Regulation
  • Genes, Tumor Suppressor
  • HMGA2 Protein
  • HeLa Cells
  • Humans
  • Mice
  • Mice, Nude
  • MicroRNAs
  • NIH 3T3 Cells
  • Neoplasms, Experimental
  • Oncogenes
  • Transfection
  • Translocation, Genetic