RAS Proteins and Their Regulators in Human Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 10 March 2026 | Viewed by 48

Special Issue Editor


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Guest Editor
Department of Radiation Oncology, UT Southwestern Medical Center, Dallas, TX 75390, USA
Interests: RAS signaling; cancer therapy; structural biology; molecular simulation
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Special Issue Information

Dear Colleagues,

RAS proteins (KRAS, NRAS, and HRAS) are small GTPases that function as binary molecular switches dependent on the loading of GTP (active state) or GDP (inactive state) and which govern critical cellular processes such as cell proliferation, differentiation, and survival. State transitions of RAS proteins are regulated either by intrinsic or GTPase-activating protein (GAP)-stimulated GTP hydrolysis or by guanine nucleotide exchange factor (GEF)-facilitated nucleotide exchange. RAS mutations are found in a large proportion of deadly human tumors, occurring in ~20–30% of malignant tumors overall. Furthermore, RAS mutations are often essential for tumor initiation and maintenance, making RAS a high-priority target in cancer therapy.

Regulators of RAS proteins, including GEFs and GAPs, play crucial roles in maintaining proper RAS signal output and preventing aberrant activation. Genetic alterations and the dysregulation of RAS regulators can contribute to oncogenesis, either by amplifying RAS signaling or reducing its suppression. Oncogenic RAS mutations usually have attenuated GTP hydrolysis, leading to an accumulation in GTP-bound form which results in the aberrant activation of RAS signaling in cancer. The most common RAS mutations occur at codons 12, 13, and 61. Efforts to directly inhibit mutant RAS proteins have established KRAS as a critical target of great importance and demonstrated that specific RAS mutants can be selectively targeted. However, challenges remain due to acquired resistance in patients.

Given the central role of RAS in cancer, targeting its signaling network remains a high priority for therapeutic intervention. As research advances, a deeper understanding of RAS regulation and function will pave the way for more effective and personalized cancer treatments.

This Special Issue will cover subjects related to recent progress in RAS proteins, RAS regulators, and their directed therapeutic approaches in cancer therapy. It aims to increase our understanding of RAS regulation and challenges in therapy targeting RAS in human cancers.

Dr. Zhiwei Zhou
Guest Editor

Manuscript Submission Information

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Keywords

  • RAS
  • RAS regulators
  • RAS-driven diseases
  • RAS-targeting therapy

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