ArticleOncotarget2017
KRAS-dependent suppression of MYC enhances the sensitivity of cancer cells to cytotoxic agents.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- RAS pathway mutations orchestrate chromatin reconfiguration and transcriptional rewiring in colorectal cancer.Cell communication and signaling : CCS · 2026Article
- KRAS and MYC synergistic inhibition: a powerful strategy targeting KRAS-mutant cancers.Molecular cancer · 2026Review
- Inverted chimeric RNAi molecules synergistically cotarget MYC and KRAS in KRAS-driven cancers.The Journal of clinical investigation · 2025Article
- Recent Progress and Potential of G4 Ligands in Cancer Immunotherapy.Molecules (Basel, Switzerland) · 2025Review
- Article
- A common druggable signature of oncogenic c-Myc, mutant KRAS and mutant p53 reveals functional redundancy and competition among oncogenes in cancer.Cell death & disease · 2024Article
- MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.Signal transduction and targeted therapy · 2024Review
- A subcomponent-guided deep learning method for interpretable cancer drug response prediction.PLoS computational biology · 2023Article
- Therapeutic Targets of KRAS in Colorectal Cancer.Cancers · 2021Review
- Article
- Ethylene glycol monomethyl ether-induced testicular oxidative stress and time-dependent up-regulation of apoptotic, pro-inflammatory, and oncogenic markers in rats.Metabolism open · 2020Article
- Methyl cellosolve-induced renal oxidative stress and time-dependent up-regulation of pro-inflammatory cytokines, apoptotic, and oncogenic markers in rats.Toxicology reports · 2020Article
- High expression of RAD51 promotes DNA damage repair and survival in KRAS-mutant lung cancer cells.BMB reports · 2019Article
- A PET Imaging Strategy for Interrogating Target Engagement and Oncogene Status in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status.Ecancermedicalscience · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
KRAS is the most commonly mutated oncogene, frequently associated with some of the deadliest forms of cancer. However, the need for potent and specific KRAS inhibitors remains unmet. Here, we evaluated the effects of selected cytotoxic agents on oncogenic KRAS signaling and drug response. The data provided new insights into the functional interaction between the KRAS and MYC pathways and revealed key differences between WT and mutant KRAS expressing cells. Systematic investigation of non-small cell lung cancer cell lines revealed that KRAS mutation can paradoxically increase the sensitivity of cells to cytotoxic agents. We identify MYC as a key regulator of the cellular stress responses and tumor cell viability as MYC expression was suppressed in drug-sensitive but not resistant cells. Furthermore, this suppression was driven by hyperactive KRAS/MAPK signaling. Our findings support a direct link between MYC and cancer cell viability, and raise the possibility that inactivation of MYC may be an effective therapeutic strategy for KRAS mutant tumors across various cancer types.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.