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Apoptosis-mediated medullary thyroid cancer growth suppression by the PI3K inhibitor LY294002

Muthusamy Kunnimalaiyaan1, Mary Ndiaye, Herbert Chen

  • 1Department of Surgery, Section of Endocrine Surgery, Endocrine Surgery Research Laboratories, The University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA.

Surgery
|December 26, 2006
PubMed
Abstract

Insights

Inhibiting the PI3K pathway in medullary thyroid cancer (MTC) reduces cell growth and neuroendocrine marker production. This suggests PI3K pathway inhibition is a potential therapeutic strategy for MTC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Signal Transduction

Background:

  • Medullary thyroid cancer (MTC) cells show activated PI3K pathway signaling.
  • Hyperactivation of Akt kinases and overexpression of neuroendocrine (NE) markers are common in MTC.

Purpose of the Study:

  • To investigate the effect of PI3K pathway inhibition on MTC cell growth.
  • To determine if PI3K inhibition reduces NE tumor marker production in MTC.

Main Methods:

  • Human MTC-TT cells were treated with the PI3K inhibitor LY294002.
  • Cellular growth and proliferation were measured.
  • Western blot analysis assessed levels of phospho-Akt, total Akt, and NE markers (CgA, ASCL1).

Main Results:

  • LY294002 significantly suppressed phospho-Akt levels in a dose-dependent manner.
  • Cellular proliferation was significantly reduced.
  • Production of NE markers (CgA, ASCL1) was decreased.
  • PI3K inhibition induced apoptosis, evidenced by increased cleaved PARP and caspase-3.

Conclusions:

  • MTC cell growth and NE marker production are dependent on PI3K signaling.
  • Inhibition of the PI3K pathway represents a potential therapeutic strategy for MTC treatment.

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