MicroRNA-490-3p regulates cell proliferation and apoptosis in gastric cancer via direct targeting of AKT1

MicroRNA-490-3p 通过直接靶向 AKT1 调控胃癌细胞增殖和凋亡

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作者:Hong Yu, Jianying Sun, Shaochang Jiang, Ying Xu

Abstract

microRNA (miRNA) expression profiles of gastric cancer (GC) and adjacent healthy gastric mucosa tissue were used to search for differentially expressed miRNAs, identifying downregulated miRNA-490-3p in GC. The present study aimed to investigate the cellular function of miRNA-490-3p and its underlying mechanism in the occurrence and progression of GC. Reverse transcription-quantitative polymerase chain reaction was used to measure miRNA-490-3p expression levels in GC tissue and adjacent healthy tissue samples. The regulatory effect of miRNA-490-3p on the proliferation and apoptosis of GC cells was detected by cell counting kit-8, colony formation assay and flow cytometry. Bioinformatic methods were used to predict AKT1 as the target of miRNA-490-3p and this was verified by a dual-luciferase reporter assay. Furthermore, western blot analysis was used to measure protein expression of AKT1 in GC cells following overexpression or knockdown of miRNA-490-3p. The present study demonstrated that miRNA-490-3p expression was downregulated in GC tissue, compared with adjacent healthy tissue. In particular, miRNA-490-3p expression levels were significantly decreased in GC tissue samples from patients with advanced cancer (stage III+IV) compared with samples from patients with early-stage (stage I+II) cancer. Additionally, miRNA-490-3p expression levels were significantly decreased in GC tissue samples from patients whose tumor size was >3 cm, compared with those <3 cm. In vitro, downregulation of miRNA-490-3p promoted cell proliferation and suppressed apoptosis. In addition, rescue experiments demonstrated that overexpression of AKT1 partially reversed the effect of miRNA-490-3p on cell proliferation and apoptosis. The present study demonstrated that miRNA-490-3p regulated proliferation and apoptosis in gastric cancer cells via direct targeting of AKT1.

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