ArticleInternational journal of immunopathology and pharmacology
Halofuginone induces ERK phosphorylation and synergizes with trametinib in gastric cancer cells.
Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe aim of this study was to investigate the effects of halofuginone (HF) on gastric cancer cells and whether the combination of HF and trametinib has synergistic effects.
introductionHalofuginone, a natural small molecule isolated from the plant
methodscell viability was performed using the CellTiterGlo assay and apoptosis and cell cycle analysis was performed by Annexin V-FITC staining and PI staining. We also analyzed RNA sequencing and differentially expressed genes was shown using the heatmap. Western blot and qPCR were carried out to determine the expression of pro-apoptotic and anti-apoptotic proteins.
resultsHF inhibited proliferation and induced apoptosis in gastric cancer cells in a dose-dependent manner. HF induced the expression of p-ERK in gastric cancer cells. HF and trametinib synergistically inhibited the gastric cancer cell proliferation. Trametinib inhibited HF-induced p-ERK expression. HF reduced anti-apoptotic protein Mcl-1 expression and reduced trametinib-induced upregulation of Mcl-1 expression.
conclusionHF exerts its anti-cancer effects in gastric cancer and has a synergistic inhibition with trametinib, which may provide a novel therapeutic strategy for gastric cancer.
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