RAS Signaling in Cancer

Dear Colleagues,

RAS signaling is involved in a wide range of biological processes such as cell proliferation, differentiation, and survival. The three human Ras genes (KRAS, NRAS, and HRAS) are the most commonly mutated oncogenes in cancer. Targeting RAS-mutant cancers with therapeutic efficaciousness remains challenging and urgently needed. Over two decades, RAS proteins have been thought undruggable due to the difficulty for small molecules to bind to the smooth surfaces of RAS proteins. The recent identification of KRAS-G12C inhibitors, however, reignites interest in the direct inhibition of RAS proteins. Alternatively, tremendous efforts have been made to target post-translational modifications of RAS, RAS regulators, and RAS effectors. Strategies designed to indirectly target RAS by improving the inhibition of RAS regulators/effectors (e.g., SHP2, RAF, and MEK inhibitors) have led to significant achievements. Additionally, important advances have also been achieved by exploiting the synthetic lethal interactions or metabolic dependencies emitted from RAS inhibition. Strategies that employ combinational therapies hold great promise to overcome drug resistance for RAS-targeted therapy.

This Special Issue welcomes submissions from diverse areas of cancer biology concerned with RAS/MAPK signaling, related vulnerabilities, and resistance mechanisms, with the purpose of stimulating intriguing perspectives that may lead to the enhanced therapeutic efficacy of treatment for RAS mutant cancers.

Dr. Jianfeng Huang
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• RAS/MAPK signaling
• cancer metabolism
• drug resistance
• targeted cancer therapy
• tumor microenvironment