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MiR-143 and MiR-145 regulate IGF1R to suppress cell proliferation in colorectal cancer

Jiaojiao Su1, Hongwei Liang2, Weiyan Yao3

  • 1Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.

Plos One
|December 5, 2014
PubMed

Insights

MicroRNAs miR-143 and miR-145 directly target and suppress Insulin-like growth factor 1 receptor (IGF1R) expression. This finding supports their role as tumor suppressors in colorectal cancer by inhibiting cell proliferation.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Insulin-like growth factor 1 receptor (IGF1R) is a tyrosine kinase receptor implicated in colorectal cancer (CRC) progression.
  • MicroRNAs (miRNAs) are key regulators of gene expression and can act as tumor suppressors or oncogenes.

Purpose of the Study:

  • To investigate the potential role of specific miRNAs in regulating IGF1R expression in colorectal cancer.
  • To identify miRNAs that directly target the IGF1R gene and to validate their functional impact on CRC cells.

Main Methods:

  • Bioinformatic analysis to predict miRNA binding sites on the IGF1R 3'-untranslated region (3'-UTR).
  • Correlation analysis of miRNA and IGF1R protein levels in colorectal cancer tissues.
  • Experimental validation using miRNA overexpression in CRC cell lines (Caco2, HT29, SW480).
  • In vitro cell proliferation assays to assess the functional consequences of IGF1R regulation.

Main Results:

  • Bioinformatic analysis identified miR-143 and miR-145 (miR-143/145) as potential regulators of IGF1R.
  • An inverse correlation was observed between miR-143/145 levels and IGF1R protein in CRC tissues.
  • Overexpression of miR-143/145 in CRC cells confirmed direct targeting of the IGF1R 3'-UTR and reduced IGF1R expression.
  • Suppression of IGF1R by miR-143/145 led to decreased proliferation of Caco2 cells.

Conclusions:

  • The miR-143/145 cluster directly targets and inhibits IGF1R translation.
  • miR-143/145 acts as a tumor suppressor in colorectal cancer by downregulating IGF1R.
  • These findings highlight a novel regulatory mechanism in colorectal cancer pathogenesis.

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