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Retinol decreases phosphatidylinositol 3-kinase activity in colon cancer cells

Eun Young Park1, Erik T Wilder, Joseph E Chipuk

  • 1Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712, USA.

Molecular Carcinogenesis
|October 6, 2007
PubMed

Insights

Retinol, a vitamin A derivative, inhibits colon cancer cell invasion by decreasing phosphatidylinositol 3-kinase (PI3K) activity. This mechanism is independent of the retinoic acid receptor and offers a potential therapeutic strategy for ATRA-resistant cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Retinol previously demonstrated inhibition of colon cancer cell invasion through a retinoic acid receptor-independent pathway.
  • Phosphatidylinositol 3-kinase (PI3K) is a key regulator of cell invasion.

Purpose of the Study:

  • To investigate whether retinol affects PI3K activity.
  • To elucidate the mechanism by which retinol influences PI3K activity and cell invasion.

Main Methods:

  • Human colon cancer cell lines (HCT-116, SW620) were treated with retinol after serum starvation.
  • PI3K activity, protein levels of PI3K subunits (p85, p110), and their heterodimerization were assessed.
  • In vitro kinase assays and computational modeling were employed to study retinol's interaction with PI3K.

Main Results:

  • Retinol significantly decreased PI3K activity in a dose-dependent manner.
  • Retinol did not affect PI3K subunit protein levels or heterodimerization.
  • Retinol's inhibition of PI3K activity was found to be similar to known PI3K inhibitors like LY294002 and wortmannin.

Conclusions:

  • Retinol inhibits colon cancer cell invasion by reducing PI3K activity.
  • This PI3K-dependent mechanism provides a novel therapeutic avenue for overcoming resistance to all-trans-retinoic acid (ATRA) in colon cancer.

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