Expression of activated PIK3CA in ovarian surface epithelium results in hyperplasia but not tumor formation

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Transplantation Into the Mouse Ovarian Fat Pad
09:25

Transplantation Into the Mouse Ovarian Fat Pad

Published on: September 7, 2016

Shun Liang1, Nuo Yang, Yue Pan

  • 1Center for Research on the Early Detection and Cure of Ovarian Cancer, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America.

Plos One
|January 28, 2009
PubMed
Abstract

Insights

Activation of Phosphatidylinositol 3'-kinase alpha (PIK3CA) alone does not transform ovarian surface epithelium (OSE). However, PIK3CA activation is crucial for maintaining OSE transformation initiated by other oncogenes like K-ras.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Phosphatidylinositol 3 -kinase (PI3K) is a critical regulator in cancer signaling pathways.
  • Genetic alterations in PIK3CA, the PI3K catalytic subunit alpha, are observed in ovarian cancer.
  • PIK3CA activation is an early event in ovarian cancer, but its role in ovarian surface epithelium (OSE) transformation is unclear.

Purpose of the Study:

  • To investigate the role of activated PIK3CA in the malignant transformation of ovarian surface epithelium (OSE).
  • To determine if PIK3CA activation can initiate OSE transformation in vivo and in vitro.

Main Methods:

  • Generated transgenic mice expressing activated PIK3CA in Müllerian epithelium using the MISIIR promoter.
  • Examined OSE hyperplasia and malignant transformation in vivo.
  • Assessed anchorage-independent growth in primary cultured OSEs, both alone and in combination with mutant K-ras.

Main Results:

  • Overexpression of activated PIK3CA in OSE induced significant hyperplasia but did not lead to malignant transformation.
  • Activated PIK3CA alone did not induce anchorage-independent growth in primary OSEs.
  • PIK3CA activation significantly enhanced anchorage-independent growth of OSEs already transformed by mutant K-ras.

Conclusions:

  • PIK3CA activation is insufficient to initiate OSE malignant transformation.
  • PIK3CA activation plays a significant role in maintaining OSE transformation initiated by other oncogenes, such as K-ras.
  • This suggests PIK3CA is a key contributor to the progression of ovarian cancer driven by other genetic events.

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