RNA-seq of neuroblastoma cells: corilagin and cisplatin sensitivity via PI3K/AKT
Drug resistance remains the leading cause of cisplatin treatment failure in neuroblastoma (NB). This study aimed to investigate the potential of corilagin as an adjuvant therapy for overcoming cisplatin resistance in NB. RNA sequencing was utilized to identify molecular mechanisms associated with cisplatin resistance and the therapeutic action of corilagin. In vitro functional assays were conducted in human NB cell lines (SH-SY5Y and SK-N-BE(2)) and a cisplatin-resistant subline (SH-SY5Y/R). RNA-seq was performed on SH-SY5Y (parental control), SH-SY5Y/R (cisplatin-resistant, treated with 10 µM cisplatin), and SH-SY5Y/R+Cor (SH-SY5Y/R co-treated with 10 µM cisplatin and 10 µM corilagin), n=3 per group. The combination of corilagin and cisplatin significantly inhibited proliferation, migration, invasion and autophagic activity in SH-SY5Y/R cells while robustly inducing apoptosis. The PI3K/AKT signaling pathway was hyperactivated during cisplatin resistance development, and corilagin suppressed this activation. Corilagin enhances cisplatin sensitivity in NB cells through modulation of the PI3K/AKT signaling pathway.