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miR-137 Targets p160 Steroid Receptor Coactivators SRC1, SRC2, and SRC3 and Inhibits Cell Proliferation

Vijay Kumar Eedunuri1, Kimal Rajapakshe1, Warren Fiskus1

  • 1Adrienne Helis Malvin Medical Research Foundation (V.K.E.), New Orleans, Louisiana 70130; and Departments of Molecular and Cellular Biology (K.R., W.F., C.G., S.A.C., C.F., S.S.S., J.S., J.S.M., C.C., B.W.O., N.M.) and Department of Medicine (W.F., C.G., S.A.C., C.F., S.S.S., J.S., J.S.M., N.M.), Baylor College of Medicine, Houston, Texas 77030.

Molecular Endocrinology (Baltimore, Md.)
|June 13, 2015
PubMed

Insights

Steroid receptor coactivators (SRCs) drive cancer growth. Restoring microRNA-137 (miR-137) levels depleted SRC expression and inhibited cancer cell proliferation, suggesting miR-137 as a potential cancer therapy.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • The p160 family of steroid receptor coactivators (SRCs) are critical regulators of gene expression implicated in cancer progression.
  • High SRC expression in cancers correlates with poor clinical outcomes and therapeutic resistance, identifying SRCs as key oncogenic drivers and therapeutic targets.
  • MicroRNAs (miRNAs) are crucial epigenetic regulators of protein expression.

Purpose of the Study:

  • To investigate the regulation of p160 SRCs by miRNAs.
  • To identify specific miRNAs targeting SRC1, SRC2, and SRC3 expression.
  • To validate the therapeutic potential of miRNA-based strategies targeting SRCs in various cancer types.

Main Methods:

  • Utilized four prediction algorithms to identify potential miRNA targets of SRC1, SRC2, and SRC3.
  • Transfected miRNA mimetics into breast cancer, uveal melanoma, and prostate cancer (PC) cell lines to assess effects on SRC protein levels and cell viability.
  • Employed reverse phase protein array analysis to identify proteins modulated by miR-137 in PC cells.

Main Results:

  • Transfection of selected miRNA mimetics effectively depleted SRC protein expression and inhibited proliferation in cancer cell lines.
  • MicroRNA-137 (miR-137) demonstrated potent depletion of SRC1, SRC2, and particularly SRC3, due to three recognition sites in the SRC3 3'-UTR.
  • miR-137 and its host gene were found to be epigenetically silenced in human cancer specimens and cell lines.

Conclusions:

  • The findings support the development of miRNA-based therapies, specifically those restoring miR-137 levels, for targeting the oncogenic p160 SRC family in cancer.
  • miR-137 exhibits significant potential as a therapeutic agent by downregulating SRC expression and inhibiting cancer cell proliferation.
  • Epigenetic silencing of miR-137 in cancers highlights its role as a tumor suppressor and a target for reactivation strategies.

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