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Phosphatidylinositol 3-kinase-dependent, MEK- independent proliferation in response to CaR activation

Tim R Bilderback1, Fred Lee, Nelly Auersperg

  • 1Department of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon 97201-3098, USA.

American Journal of Physiology. Cell Physiology
|June 11, 2002
PubMed

Insights

Elevated calcium activates phosphatidylinositol 3-kinase (PI3K) in ovarian cells, driving proliferation independently of extracellular signal-regulated kinase (ERK) signaling. This PI3K pathway is crucial for ovarian surface epithelial cell growth.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Ovarian surface epithelial (OSE) cells are implicated in most ovarian tumors.
  • Regulatory pathways controlling OSE cell proliferation remain poorly understood.

Purpose of the Study:

  • To investigate the role of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) in calcium-induced proliferation of OSE cells.

Main Methods:

  • Treatment of OSE cells with elevated extracellular calcium.
  • Inhibition of PI3K and ERK pathways using specific inhibitors (wortmannin, LY-294002, PD-98059).
  • Assessment of ERK activation and cell proliferation assays.
  • Expression of dominant-negative PI3K.

Main Results:

  • Elevated calcium activates PI3K in OSE cells.
  • PI3K inhibition significantly reduced calcium-induced proliferation (>90%), while ERK inhibition had a lesser effect (~50%).
  • PI3K is essential for ERK activation in response to calcium.

Conclusions:

  • Calcium-induced OSE cell proliferation involves both ERK-dependent and ERK-independent pathways.
  • The ERK-independent pathway is critically dependent on PI3K activation.
  • PI3K plays a dominant role in regulating calcium-mediated OSE cell proliferation.

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