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HIPK2 reduces the resistance of gastric cancer cells to cisplatin via p53 pathway
Abstract
Purpose: To uncover the functional effect of homologous domain-associated protein kinase 2 (HIPK2) on the viability of cisplatin (DDP)-resistant gastric cancer (GC) cells and elucidate the possible mechanism of action.
Methods: The effect of DDP on GC viability and apoptotic rate was evaluated using MTT and flow cytometry (FCM) assays. The potential effect of HIPK2 on DDP sensitivity and cell apoptosis was investigated in the presence of cisplatin while the effect of HIPK2 on p53 activation was determined by immunoblot assay.
Results: HIPK2 expression was decreased in DDP-resistant GC cell while upregulation of HIPK2 reduced growth, but promoted apoptosis in DDP-resistant GC cells. Further investigations showed that HIPK2 promoted p53 activation, while suppression of p53 weakened the inhibitory effect of HIPK2 on DDP-resistance in GC cells.
Conclusion: The results suggest that HIPK2 is a promising and important therapeutic factor for the regulation of the resistance of GC cells to DDP. Thus, may have a role to play in the management of gastric cancer
Keywords: Gastric cancer, Cisplatin, HIPK2, Homologous domain-associated protein kinase 2, p53 pathway, Therapeutic target
