MCM3AP‑AS1 promotes cisplatin resistance in gastric cancer cells via the miR‑138/FOXC1 axis

Abstract

The dysregulation of long non‑coding RNAs (lncRNAs) serves a pivotal role in the pathogenesis and devel‑ opment of multiple types of human cancer, including gastric cancer (GC). MCM3AP‑antisense 1 (MCM3AP‑AS1) has been reported to function as a tumor promoter in various types of cancer. However, the biological function of MCM3AP‑AS1 in the resistance of GC cells to cisplatin (CDDP) remains to be elucidated. The present study aimed to elucidate the mecha‑ nisms of MCM3AP‑AS1 in the resistance of GC cells to CDDP. The expression levels of MCM3AP‑AS1, miR‑138 and FOXC1 were measured via reverse transcription‑quantitative PCR. In addition, cell viability, migration and invasion were assessed via the Cell Counting Kit‑8, wound healing and transwell assays, respectively. The interaction between genes was confirmed via the dual‑luciferase reporter and pull‑down assays. Western blot analysis was performed to detect FOXC1 protein expression. In the present study, it was demonstrated that MCM3AP‑AS1 expression was upregulated in CDDP‑resistant GC cells and that MCM3AP‑AS1‑knockdown suppressed CDDP resistance in GC cells. Moreover, the examination of the molecular mechanism indicated that MCM3AP‑AS1 upregulated FOXC1 expression by sponging microRNA (miR)‑138. Additionally, it was identified that the overexpression of FOXC1 abolished MCM3AP‑AS1‑knockdown‑ or miR‑138 mimic‑mediated inhibitory effects on CDDP resistance in GC cells. In conclu‑ sion, the present findings suggested that MCM3AP‑AS1 enhanced CDDP resistance by sponging miR‑138 to upregu‑ late FOXC1 expression, indicating that MCM3AP‑AS1 may be a novel promising biomarker for the diagnosis and treatment of patients with GC.