Target intelligence / Profile preview

Myc proto-oncogene protein (MYC) and Ras proto-oncogene GTPase family (RAS)

Molecular classification
Transcription factor, GTPase, Oncogene
01

Overview

Cancer cell transcription of c-myc and c-ras proto-oncogenes refers to the biological processes that regulate the expression of two major drivers of oncogenesis: the MYC transcription factor and the RAS family of GTPases. MYC (c-Myc) is a master regulator of the genome, controlling genes essential for cell cycle progression, metabolism, and protein synthesis (Source: UniProt P01106). The RAS family (including KRAS, HRAS, and NRAS) acts as a molecular switch in signaling pathways that promote cell survival and growth (Source: UniProt P01116). In many cancers, these genes are overexpressed or mutated, leading to constitutive activity and tumor progression. Therapeutic approaches to inhibit their transcription include BET bromodomain inhibitors like JQ1, which prevent the assembly of the transcriptional complex at the MYC promoter, and G-quadruplex stabilizers like CX-5461, which impede RNA polymerase by stabilizing DNA secondary structures (Source: PubMed 20946927, 28249918). Because these genes are also vital for normal tissue regeneration, targeting their transcription presents significant challenges regarding systemic toxicity and the therapeutic window.

Other names
c-Mycc-RasMYCKRASHRASNRASCancer cell transcription of c-myc and c-ras proto-oncogenes
02

Mechanism of action

Inhibition of gene expression through epigenetic modulation of bromodomains, stabilization of promoter G-quadruplex structures, or antisense-mediated mRNA degradation.

03

Biological functions

Cell proliferationCell cycleSignal transductionApoptosis
04

Disease associations

Cancer
05

Safety considerations

Systemic toxicityBone marrow suppressionGastrointestinal toxicityNarrow therapeutic index
06

Interacting drugs

JQ1

5 more in the full profile.

07

Biomarkers

MYC amplificationKRAS mutationNRAS mutationHRAS mutation

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