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Active RAC1 Promotes Tumorigenic Phenotypes and Therapy Resistance in Solid Tumors

Pradip De1,2, Brett James Rozeboom3, Jennifer Carlson Aske1

  • 1Translational Oncology Laboratory, Avera Cancer Institute, Sioux Falls, SD 57105, USA.

Cancers
|June 18, 2020
PubMed

Insights

Ras-related C3 botulinum toxin substrate 1 (RAC1) acts as a molecular switch in cancer. RAC1 hyperactivation drives tumor progression and therapy resistance in solid tumors by promoting proliferation, EMT, and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Guanosine triphosphate (GTP)-ase family members, including RAC1, Rho, and Cdc42, are implicated in oncogenic transformations in solid tumors.
  • RAC1 alterations, such as hyperactivation and copy-number gain, are frequently observed in various solid cancers.
  • RAC1 is recognized for its critical role in tumor progression and the development of therapeutic resistance.

Purpose of the Study:

  • To review the frequency and functional roles of Ras-related C3 botulinum toxin substrate 1 (RAC1) alterations in diverse cancers.
  • To investigate the multifaceted functions of RAC1 in solid tumors, focusing on tumor progression and therapeutic resistance.
  • To emphasize RAC1's involvement in specific tumor cell phenotypes, including apoptosis inhibition, proliferation, epithelial-to-mesenchymal transition (EMT), stemness, angiogenesis, and metastasis.

Main Methods:

  • Literature review and analysis of existing data on RAC1 alterations in adult solid tumors.
  • Examination of RAC1's functional mechanisms contributing to tumor cell phenotypes.
  • Summarization of RAC1's role in mediating resistance to cancer therapies.

Main Results:

  • RAC1 hyperactivation and copy-number gains are common features in solid tumors.
  • RAC1 significantly contributes to tumor progression by influencing proliferation, apoptosis, EMT, stemness, angiogenesis, and metastasis.
  • RAC1 plays a contextual role in the development of resistance to various clinical cancer therapies.

Conclusions:

  • RAC1 is a key molecular player in the progression of adult solid tumors.
  • Understanding RAC1's diverse functions is crucial for developing strategies to overcome therapeutic resistance.
  • Targeting RAC1 pathways may offer novel therapeutic avenues for managing solid tumors.
Keywords:
CSCEMTRAC1angiogenesisapoptosisinvasionmetastasisproliferationresistancesolid tumors

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