Related Experiment Video

Updated: Feb 4, 2026

An Orthotopic Model of Serous Ovarian Cancer in Immunocompetent Mice for in vivo Tumor Imaging and Monitoring of Tumor Immune Responses
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An Orthotopic Model of Serous Ovarian Cancer in Immunocompetent Mice for in vivo Tumor Imaging and Monitoring of Tumor Immune Responses

Published on: November 28, 2010

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Ovarian Tumor Microenvironment Signaling: Convergence on the Rac1 GTPase

Laurie G Hudson1,2, Jennifer M Gillette3,4, Huining Kang5,6

  • 1Department of Pharmaceutical Sciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. lhudson@salud.unm.edu.

Cancers
|September 29, 2018
PubMed

Insights

The small GTPase Ras-related C3 botulinum toxin substrate (Rac)1 plays a key role in ovarian cancer progression and metastasis. Targeting Rac1 may offer new therapeutic strategies for epithelial ovarian cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The tumor microenvironment (TME) in epithelial ovarian cancer (EOC) is complex, featuring bioactive molecules that influence cell interactions and signaling pathways.
  • These signals impact tumor progression, metastasis, and response to therapy.
  • Many signaling pathways converge on the small GTPase Ras-related C3 botulinum toxin substrate (Rac)1.

Purpose of the Study:

  • To review evidence of Rac1 activation in the ovarian TME.
  • To discuss mechanisms of Rac1 dysregulation in ovarian cancer.
  • To explore the potential benefits of targeting Rac1 in this disease.

Main Methods:

  • Literature review of studies on Rac1 in ovarian cancer.
  • Analysis of Rac1's role in TME signaling.
  • Examination of Rac1's downstream effectors and their impact on tumor behavior.

Main Results:

  • Rac1 regulates actin cytoskeleton remodeling, crucial for tumor cell adhesion, migration, and invasion.
  • Rac1 influences cancer cell survival, tumor angiogenesis, phenotypic plasticity, quiescence, and therapeutic resistance.
  • Evidence suggests Rac1 activation and dysregulation within the ovarian TME.

Conclusions:

  • Rac1 is a critical regulator of multiple processes in ovarian cancer.
  • Targeting aberrant Rac1 activity presents a potential therapeutic strategy.
  • Rac1 may contribute to the extraperitoneal dissemination of ovarian cancer.
Keywords:
GTPase activating proteins (GAPs)Rac1Rho-GTPasebone nicheguanine nucleotide exchange factors (GEFs)oncogeneoncoproteinovarian cancertherapeutic targetingtumor microenvironment

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