MicroRNA3650 Promotes Gastric Cancer Proliferation and Migration through the PTEN/PI3K-AKT-mTOR and Hippo Pathways.

IF 1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Protein and Peptide Letters Pub Date : 2023-01-01 DOI:10.2174/0109298665265642231020043809
Xiansheng Yang, Juncai Wen, Qingjun He, Shuoshan Wang, Qiang Ruan, Quanxing Liao, Jinfu He, Shuxian Fang, Chang Liu, Hongsheng Tang
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Abstract

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.

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MicroRNA3650通过PTEN/PI3K-AKT-mTOR和Hippo途径促进胃癌增殖和迁移。
背景:胃癌是一种预后严重不良的恶性肿瘤。研究表明,microRNAs (miRNAs)在GC中起着多方面的调控作用。然而,miR-3650在胃癌进展中的作用尚不清楚。方法:本研究采用临床标本检测miR-3650的表达及其临床意义。通过CCK-8、细胞划痕和transwell实验,在胃癌细胞系中检测miR-3650的生物学功能。生物信息学预测结合Western blot实验,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,为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,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通路在胃癌的进展中至关重要,可以作为胃癌治疗的新靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Protein and Peptide Letters
Protein and Peptide Letters 生物-生化与分子生物学
CiteScore
2.90
自引率
0.00%
发文量
98
审稿时长
2 months
期刊介绍: Protein & Peptide Letters publishes letters, original research papers, mini-reviews and guest edited issues in all important aspects of protein and peptide research, including structural studies, advances in recombinant expression, function, synthesis, enzymology, immunology, molecular modeling, and drug design. Manuscripts must have a significant element of novelty, timeliness and urgency that merit rapid publication. Reports of crystallization and preliminary structure determination of biologically important proteins are considered only if they include significant new approaches or deal with proteins of immediate importance, and preliminary structure determinations of biologically important proteins. Purely theoretical/review papers should provide new insight into the principles of protein/peptide structure and function. Manuscripts describing computational work should include some experimental data to provide confirmation of the results of calculations. Protein & Peptide Letters focuses on: Structure Studies Advances in Recombinant Expression Drug Design Chemical Synthesis Function Pharmacology Enzymology Conformational Analysis Immunology Biotechnology Protein Engineering Protein Folding Sequencing Molecular Recognition Purification and Analysis
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