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Regulation of survivin expression by IGF-1/mTOR signaling

V Vaira1, C W Lee, H L Goel

  • 1Department of Cancer Biology and the Cancer Center, University of Massachusetts Medical School, Worcester, MA 01605, USA, and AOS Paolo and Fondazione Ospedale Maggiore Policlinico, Regina Elena and Mangiagalli, Milan, Italy.

Oncogene
|October 31, 2006
PubMed

Insights

Insulin-like growth factor-1 (IGF-1) boosts survivin protein in prostate cancer cells by enhancing mRNA translation via the mTOR pathway. Inhibiting this pathway may offer a new cancer therapy strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • Survivin is overexpressed in many human tumors, regulating cell proliferation and viability.
  • Understanding survivin's regulatory mechanisms is crucial for developing targeted cancer therapies.
  • The precise molecular pathways controlling survivin expression in tumors remain incompletely understood.

Purpose of the Study:

  • To investigate the role of insulin-like growth factor-1 (IGF-1) in regulating survivin expression in prostate cancer cells.
  • To elucidate the molecular mechanisms by which IGF-1 influences survivin levels.
  • To explore the therapeutic potential of targeting the IGF-1 signaling pathway in prostate cancer.

Main Methods:

  • Stimulation of prostate cancer cells with IGF-1.
  • Assessment of survivin expression, mRNA levels, and protein stability.
  • Inhibition of the mammalian target of rapamycin (mTOR) pathway using rapamycin.
  • Manipulation of p70S6K1 expression using forced expression and small interfering RNA (siRNA).
  • Evaluation of cell viability under different treatment conditions.

Main Results:

  • IGF-1 stimulation increased survivin expression in prostate cancer cells.
  • This increase was independent of gene transcription, mRNA levels, or protein stability.
  • IGF-1 enhanced survivin mRNA translation, a process dependent on the mTOR pathway.
  • The mTOR target p70S6K1 was identified as a key mediator of IGF-1-induced survivin upregulation.
  • Rapamycin treatment reduced survivin levels and prostate cancer cell viability, both alone and in combination with taxol.

Conclusions:

  • The IGF-1/mTOR signaling pathway rapidly elevates survivin expression in prostate cancer cells through enhanced mRNA translation.
  • Targeting the IGF-1/mTOR pathway, potentially with rapamycin, could lower survivin levels and decrease prostate cancer cell viability.
  • Inhibiting this pathway may be a promising therapeutic strategy to overcome survivin-mediated anti-apoptotic resistance in prostate cancer.

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