Transcriptomic Profiling of Kinase Inhibitor Treated Cancer Cell Lines Reveals Insights into Drug Response Mechanisms

Protein kinases regulate essential cellular processes, including growth, differentiation, and apoptosis, and their dysregulation is implicated in cancer progression. Kinase inhibitors have emerged as critical therapeutic agents; however, challenges such as drug resistance and selectivity gaps necessitate further investigation. To address these challenges, we performed RNA sequencing-based transcriptomic profiling to assess the impact of targeted kinase inhibitors on cancer cells. Specifically, we analyzed the gene expression changes induced by Tepotinib (1 μM) in GSC923 glioblastoma cells, Gilteritinib (1 μM) in MDA-MB-231 triple-negative breast cancer cells, and Brigatinib (1 μM) in PANC-1 pancreatic cancer cells. Wild-type (WT) untreated controls were included for comparative analysis. RNA sequencing was conducted using a paired-end strategy, and differential gene expression analysis was performed to uncover treatment-induced transcriptional alterations. This dataset provides insights into the molecular mechanisms of kinase inhibitor response, highlighting potential repurposing opportunities and informing future therapeutic strategies in glioblastoma, breast cancer, and pancreatic cancer.