ArticleCancer chemotherapy and pharmacology2025
Anti-tumor efficacy of RAF/MEK inhibitor VS6766 in KRAS-mutated colorectal cancer cells.
Article in Cancer chemotherapy and pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Targeted therapy for KRAS G12C-mutated colorectal cancer: advances, challenges, and future directions.American journal of cancer research · 2025Review
- Combination treatment with RAF/MEK inhibitor avutometinib and FAK inhibitor defactinib in preclinical models of meningioma.Neuro-oncology advancesArticle
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Authors and funding
9 authors.
Funding
Abstract
purposeColorectal cancer (CRC) ranks third among most prevalent cancers worldwide. KRAS is the most frequently (30-40%) mutated oncogene in CRC, which has been defined as an "undruggable" therapeutic target over the past four decades.
methodsIn this study, we applied four HT-29 cell lines, namely HT-29-wild-type (HT-29-WT), point-mutated HT-29-KRAS
resultsTreatment with VS6766 inhibited the proliferation of all four HT29 cells, while PLX4720 had a modest inhibitory effect. VS6766 induced G1-phase arrest as well as cell apoptosis, accompanied by the downregulation of p-ERK and p-MEK. Moreover, VS6766 and 5-FU synergistically suppressed HT-29 cells' growth. Meanwhile, p-AKT was upregulated after VS6766 treatment. The AKT inhibitor MK2206 and VS6766 showed synergistic effect in all four cell lines.
conclusionTaken together, this study provides the first experimental evidence to demonstrate that all G12 mutation cell lines are sensitive to VS6766 applied either alone or combined with 5-FU or AKT inhibitor.
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