HCP5 Promotes Proliferation and Contributes to Cisplatin Resistance in Gastric Cancer Through miR-519d/HMGA1 Axis

Introduction: The long-non-coding RNA HCP5 (HLA complex P5) has been extensively linked to the ability of cancer cells to resist chemotherapeutic interventions. Here, we investigated the role of HCP5 in gastric cancer (GC) which to-date has been poorly characterized. Our results indicated that HCP5 expression was up-regulated in GC cells. Methods: HCP5, miR-519d, and high mobility group A1 (HMGA1) expression levels in GC cells were measured using quantitative real-time PCR (qRT-PCR) and Western blot analysis. Drug sensitivity and apoptosis of tumor cells were assessed using cell counting kit8, flow cytometry, and caspase activity assay. Bioinformatics and luciferase reporter assays were employed for analyzing the interactions between HCP5, miR-519d, and HMGA1. Results: HCP5 knockdown suppressed proliferation and weakened the resistance to cisplatin (DDP) of GC cells. miR-519d was down-regulated in GC cells and sponged by HCP5. HMGA1 was directly inhibited by miR-519d and its expression was up-regulated in GC cells. HCP5 exacerbated the resistance to cisplatin of GC cells in vitro by enhancing HMGA1 expression via sponging miR-519d. Conclusion: In summary, HCP5 promoted proliferation and contributed to DDP resistance in GC cells through miR-519d/HMGA1 axis.

Automated summary

HCP5 promoted proliferation and contributed to cisplatin resistance in gastric cancer cells through the miR-519d/HMGA1 axis.