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An expanding role for RAS GTPase activating proteins (RAS GAPs) in cancer

Ophélia Maertens1, Karen Cichowski2

  • 1Genetics Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA.

Advances in Biological Regulation
|May 13, 2014
PubMed

Insights

RAS GTPase Activating Proteins (RAS GAPs) are emerging tumor suppressors. Their inactivation can activate RAS, contributing to cancer, even without RAS mutations. Further research is needed on their roles.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The RAS pathway is frequently deregulated in human cancers, with RAS gene mutations found in nearly 30% of tumors.
  • Hyperactivation of RAS and downstream pathways occurs in some cancers lacking RAS mutations.
  • RAS GTPase Activating Proteins (RAS GAPs) are a class of tumor suppressors that inactivate RAS.

Purpose of the Study:

  • To review the current understanding of RAS GAPs in human disease.
  • To explore the emerging role of RAS GAPs as tumor suppressors.
  • To highlight outstanding questions regarding RAS GAP function and cancer relevance.

Main Methods:

  • Literature review of RAS GAPs in human disease.
  • Analysis of the role of RAS GAPs in cancer development.
  • Discussion of the differential functions of RAS GAP family members.

Main Results:

  • Inactivation of RAS GAPs provides an alternative mechanism for RAS pathway activation in cancer.
  • Loss of RAS GAP function, exemplified by NF1, promotes excessive RAS activation and tumor predisposition.
  • The human genome contains 13 additional RAS GAP family members with largely uncharacterized roles in cancer.

Conclusions:

  • RAS GAPs are critical regulators of the RAS pathway and represent an important class of tumor suppressors.
  • Understanding the diverse functions of the RAS GAP family is crucial for comprehending their collective role in human cancer.
  • Further investigation into RAS GAPs is warranted to elucidate their full potential in cancer diagnosis and therapy.
Keywords:
DAB2IPGAPGTPase activating proteinIQGAPNF1RASRAS GAPRASAL2Therapeutic resistance

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