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The Function of RAS Mutation in Cancer and Advances in its Drug Research

Shijie Chen1, Fengyang Li1, Dan Xu1

  • 1State Key Laboratory of Natural Medicines, Department of Physiology, China Phar maceutical University, Nanjing 210009, China.

Current Pharmaceutical Design
|May 7, 2019
PubMed

Insights

RAS proteins are key drivers in many cancers. Current RAS inhibitors face challenges, suggesting that targeting multiple pathways simultaneously is a promising therapeutic strategy for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • RAS genes (H-ras, K-ras, N-ras) are frequently mutated in human cancers, acting as critical oncogenic drivers.
  • RAS proteins mediate extracellular signals into intracellular cascades, regulating cell proliferation, apoptosis, metabolism, and angiogenesis via pathways like MAPK and PI3K.
  • Existing treatments for RAS-driven cancers, including direct and pathway inhibitors, are limited by resistance and off-target toxicity.

Purpose of the Study:

  • To review the role of normal and mutant RAS genes in cancer development.
  • To elucidate RAS-regulating signaling pathways.
  • To highlight advancements in RAS inhibitor research and identify future therapeutic directions.

Main Methods:

  • Literature review and analysis of the role of RAS genes in cancer.
  • Elucidation of RAS-mediated signaling pathways.
  • Review of current and emerging RAS inhibitor strategies.

Main Results:

  • RAS mutations are central to oncogenesis, influencing multiple cellular processes.
  • RAS signaling pathways are complex and interconnected.
  • Current RAS inhibitor approaches show limitations, necessitating novel strategies.

Conclusions:

  • Single-target inhibition in RAS pathways may be insufficient due to pathway crosstalk.
  • Combined multi-target drug approaches offer a promising strategy for overcoming resistance and toxicity.
  • Future research should focus on compensatory mechanisms and combination therapies for RAS-driven cancers.
Keywords:
KRASRAS mutationcancerinhibitorsignal pathwaytargeted drug.

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