Riccardin D, a drug candidate, inhibits gastric cancer progression by targeting RAD54L

Abstract

Purpose: To investigate the beneficial function of RAD54L in gastric cancer. Methods: Batch correction, metaboanalyst, volcano plot and heatmap were used for analyzing different expression genes. Metascape and strings were used for functional enrichment and protein-protein interaction network analysis, respectively. Expression of RAD54L was analyzed using online platform-timer, ualcan and GEPIA. Correlation between RAD54L and poor prognosis was analyzed using Kaplan-Meier curve. Expression of RAD54L was evaluated by Real Time-quantitative PCR and western blotting, while cell proliferation, cell apoptosis and cell cycle were determined by CCK8 and flow cytometry, respectively. Results: A total of 57 upregulated DEGs and 33 downregulated DEGs were involved in gastric cancer. Among these, RAD54L was a hub gene which is highly expressed, and is related to poor survival in gastric cancer. Moreover, knockdown of RAD54L inhibited cell viability and facilitated cell apoptosis in gastric cancer cells (p < 0.05). On the other hand, overexpression of RAD54L promoted cell proliferation and reduced cell apoptosis in gastric cancer (p < 0.05). In addition, RAD54L positively regulated cell cycle in gastric cancer cell lines. Furthermore, riccardin D negatively regulated cell cycle in gastric cancer cell lines by targeting RAD54L. Conclusion: Riccardin DRAD54L is a potential drug for the treatment of gastric cancer. However, developmental work, including in vivo studies, are required to ascertain this.