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RAS is regulated by the let-7 microRNA family.

MicroRNAs (miRNAs) are regulatory RNAs found in multicellular eukaryotes, including humans, where they are implicated in cancer. The let-7 miRNA times seam cell terminal differentiation in C. elegans. Here we show that the let-7 family negatively regulates let-60/RAS. Loss of let-60/RAS suppresses let-7, and the let-60/RAS 3'UTR contains multiple let-7 complementary sites (LCSs), restricting reporter gene expression in a let-7-dependent manner. mir-84, a let-7 family member, is largely absent in vulval precursor cell P6.p at the time that let-60/RAS specifies the 1 degrees vulval fate in that cell, and mir-84 overexpression suppresses the multivulva phenotype of activating let-60/RAS mutations. The 3'UTRs of the human RAS genes contain multiple LCSs, allowing let-7 to regulate RAS expression. let-7 expression is lower in lung tumors than in normal lung tissue, while RAS protein is significantly higher in lung tumors, providing a possible mechanism for let-7 in cancer.

Pubmed ID: 15766527


  • Johnson SM
  • Grosshans H
  • Shingara J
  • Byrom M
  • Jarvis R
  • Cheng A
  • Labourier E
  • Reinert KL
  • Brown D
  • Slack FJ



Publication Data

March 11, 2005

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM62594
  • Agency: NIGMS NIH HHS, Id: R01 GM062594

Mesh Terms

  • 3' Untranslated Regions
  • Animals
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Carcinoma
  • Cell Differentiation
  • Cell Lineage
  • Cell Transformation, Neoplastic
  • Down-Regulation
  • Gene Expression Regulation, Developmental
  • Genes, Reporter
  • HeLa Cells
  • Humans
  • Lung Neoplasms
  • MicroRNAs
  • Molecular Sequence Data
  • ras Proteins