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Let-7a regulation of insulin-like growth factors in breast cancer

Lingeng Lu1, Dionyssios Katsaros, Yong Zhu

  • 1Department of Epidemiology and Public Health, Yale Cancer Center, Yale University School of Medicine, 60 College Street, New Haven, CT 06520-8034, USA.

Breast Cancer Research and Treatment
|September 18, 2010
PubMed

Insights

Methylated let-7a-3 microRNA is common in breast cancer, inversely correlating with Insulin-like Growth Factor (IGF) expression. Unlike other oncogenes, let-7a may up-regulate IGFs in cancer cells.

Area of Science:

  • Epigenetics
  • Molecular Oncology
  • Gene Regulation

Background:

  • DNA methylation regulates microRNA gene expression, impacting downstream molecules.
  • Previous research linked methylated let-7a-3 to low IGF-II and better ovarian cancer prognosis.
  • The role of let-7a-3 methylation in breast cancer and IGF regulation remained unclear.

Purpose of the Study:

  • To investigate the role of let-7a-3 methylation in breast cancer.
  • To analyze the association between let-7a-3 methylation and Insulin-like Growth Factor (IGF) expression.
  • To determine the relationship between let-7a-3 methylation, tumor features, and patient survival.

Main Methods:

  • Analysis of let-7a-3 methylation, IGF mRNAs, and peptides in 348 breast cancer samples using quantitative methylation-specific PCR, qRT-PCR, and ELISA.
  • In vitro experiments with HeLa cells transfected with let-7a precursors.
  • Statistical analysis of associations with disease features and survival.

Main Results:

  • Let-7a-3 methylation was frequently detected in breast cancer, inversely correlating with IGF expression.
  • In vitro studies indicated let-7a can increase IGF expression in cancer cells with low endogenous let-7a.
  • Methylation was associated with high-grade, ER-/PR-negative tumors but not patient survival.

Conclusions:

  • Epigenetic regulation of let-7a-3 influences IGF actions in breast cancer.
  • Let-7a may up-regulate IGF expression in cancer cells, differing from its effects on other oncogenes.
  • Further research into let-7a-3 methylation and IGF pathways in cancer is warranted.

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