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Ras-mediated activation of mTORC2 promotes breast epithelial cell migration and invasion

Shannon E Collins1, Mollie E Wiegand1, Alyssa N Werner1

  • 1Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721.

Molecular Biology of the Cell
|December 21, 2022
PubMed

Insights

The Ras-mTORC2 pathway drives breast cancer cell migration and invasion. While Ras-mediated mTORC2 activation has a minor role in tumor formation, it is crucial for cancer cell spread.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Mechanistic target of rapamycin complex 2 (mTORC2) is a key regulator of cell migration.
  • Ras proteins are known to control cell migration and are implicated in cancer.
  • mTORC2 has been linked to cancer cell migration, particularly in breast cancer.

Purpose of the Study:

  • To investigate the role of Ras in breast cancer cell migration and invasion via mTORC2.
  • To determine if Ras-mediated mTORC2 activation contributes to breast cancer progression.

Main Methods:

  • Utilized breast cancer cell lines and models, including HER2 and oncogenic Ras-transformed MCF10A cells.
  • Assessed the impact of Ras and mTORC2 on cell migration and invasion.
  • Investigated the effect of disrupting mTORC2 on cancer cell proliferation and invasiveness.

Main Results:

  • Both Ras and mTORC2 were found to promote the migration of various breast cancer cells.
  • Wild-type and oncogenic Ras activate mTORC2, leading to mTORC2-dependent migration and invasion in breast cancer models.
  • Disruption of mTORC2 abolished invasiveness in oncogenic Ras-transformed cells, while proliferation remained uncontrolled.

Conclusions:

  • The Ras-mTORC2 pathway is a significant driver of breast cancer cell migration and invasion.
  • Ras-mediated mTORC2 activation plays a minor role in breast tumor formation but is critical for metastatic processes.

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