Hesperadin sensitizes gastric cancer cells to cisplatin via NOX1-dependent oxidative stress.

ABSTRACT: The therapeutic efficacy of cisplatin in gastric cancer (GC) is frequently constrained by chemoresistance and systemic toxicity. Targeted small molecules hold promise for providing synergistic effects that enhance treatment outcomes. GC cell viability was assessed via a Cell Counting Kit-8 (CCK-8) assay. Apoptosis, intracellular reactive oxygen species (ROS) levels, and the mitochondrial membrane potential were evaluated via flow cytometry and JC-1 staining. Transcriptomic analysis [RNA-sequencing (RNA-Seq)] was subsequently conducted to identify differentially regulated pathways, followed by validation via reverse transcription-quantitative PCR and western blotting. DNA damage was measured by γ-H2AX immunofluorescence, and clonogenic survival was examined. The NOX1-specific inhibitor ML17

SUBMITTER: Zhu W 

PROVIDER: S-EPMC12598528 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature