Background:: Gastric cancer (GC) is a malignant tumor with seriously poor outcomes. Studies have shown that microRNAs (miRNAs) play an omnifarious regulatory effect in GC. However, the role of miR-3650 in the progression of GC is not well known. Methods:: In this study, miR-3650 expression and its clinical significance were determined using clinical specimens. The biological functions of miR-3650 were determined in gastric cancer cell lines through CCK-8, cell scratch, and transwell experiments. Bioinformatics predictions, combined with Western blot experiments, were employed to explore its downstream molecular targets. Results:: We observed that miR-3650 was overexpressed in GC specimens and most cell lines, i.e., 77.8% (MKN28, SNU1, AGS, MKN45, N87, BGC823 and SGC7901). The overexpression correlated with advanced T-stage, N-stage, M-stage, and TNM-stage. Furthermore, miR-3650 promoted the proliferation and migration of gastric cancer cells, and its overexpression promoted the PI3K-AKT-mTOR pathway and inhibited the PTEN and hippo pathways. The potassium ion signaling pathway was also involved in the biological process of miR-3650 promoting cancer. Conclusion:: Therefore, we concluded that miR-3650/PTEN/PI3K-AKT-mTOR and miR-3650/hippo pathways are vital in the progression of GC and serve as novel targets for GC therapy.

中文翻译：

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MicroRNA3650 通过 PTEN/PI3K-AKT-mTOR 和 Hippo 通路促进胃癌增殖和迁移

背景：胃癌（GC）是一种预后极差的恶性肿瘤。研究表明，微小RNA（miRNA）在GC中发挥全方位的调控作用。然而，miR-3650 在 GC 进展中的作用尚不清楚。方法:: 在本研究中，使用临床标本确定 miR-3650 的表达及其临床意义。通过 CCK-8、细胞划痕和 Transwell 实验确定了 miR-3650 在胃癌细胞系中的生物学功能。采用生物信息学预测结合蛋白质印迹实验来探索其下游分子靶点。结果：我们观察到 miR-3650 在 GC 标本和大多数细胞系中过表达，即 77.8%（MKN28、SNU1、AGS、MKN45、N87、BGC823 和 SGC7901）。过表达与晚期 T 期、N 期、M 期和 TNM 期相关。此外，miR-3650促进胃癌细胞的增殖和迁移，其过表达促进PI3K-AKT-mTOR通路并抑制PTEN和hippo通路。钾离子信号通路也参与了miR-3650促癌的生物学过程。结论：因此，我们得出结论，miR-3650/PTEN/PI3K-AKT-mTOR 和 miR-3650/hippo 通路在 GC 进展中至关重要，可作为 GC 治疗的新靶点。