MiR-124-3p inhibits proliferation, migration, and epithelial-mesenchymal transformation in gastric cancer by targeting ITGB1.

IF 1.7 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
American journal of translational research Pub Date : 2025-04-15 eCollection Date: 2025-01-01 DOI:10.62347/AJPA6532
Qiuhao Li, Li Zhou, Qiong Liang, Huaxin Qin, Yao Chen, Tiancheng Wang, Qian Wei, Yuanyun Luo, Guanghao Li, Haige Huang
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引用次数: 0

Abstract

Objective: To investigate the functional interaction between miR-124-3p and integrin β1 (ITGB1) in gastric cancer.

Methods: A comprehensive approach integrating bioinformatic prediction with experimental validation was employed. The study used dual luciferase reporter assay, CCK-8 assay, RT-qPCR, western blotting, wound healing assay, and transwell assays to systematically investigate the role of the miR-124-3p/ITGB1 regulatory axis in gastric cancer cell models.

Results: This study identified a novel regulatory axis involving miR-124-3p and ITGB1. Mechanistic investigations demonstrated that miR-124-3p directly targets ITGB1, as confirmed by dual-luciferase reporter assays. Aberrant expression of miR-124-3p significantly suppressed ITGB1 mRNA and protein levels, leading to impaired oncogenic properties, including reduced proliferation, migration, and invasion of gastric cancer cells. Furthermore, ITGB1 downregulation inhibited gastric cancer cell growth and invasion while suppressing epithelial-mesenchymal transformation (EMT). Notably, key EMT regulators, such as E-cadherin, were up-regulated. These findings suggest that miR-124-3p-mediated ITGB1 downregulation effectively suppresses gastric cancer progression by inhibiting cell proliferation, invasion, and metastasis.

Conclusions: miR-124-3p functions as a tumor-suppressive miRNA that inhibits gastric cancer development through targeting ITGB1. The miR-124-3p/ITGB1 axis provides novel insight and may serve as a promising biomarker for gastric cancer diagnosis and treatment.

MiR-124-3p通过靶向ITGB1抑制胃癌的增殖、迁移和上皮-间质转化。
目的:探讨miR-124-3p与整合素β1 (ITGB1)在胃癌中的功能相互作用。方法:采用生物信息学预测与实验验证相结合的综合方法。本研究采用双荧光素酶报告基因法、CCK-8法、RT-qPCR、western blotting法、创面愈合法、transwell法等方法,系统探讨miR-124-3p/ITGB1调控轴在胃癌细胞模型中的作用。结果:本研究发现了一个涉及miR-124-3p和ITGB1的新的调控轴。机制研究表明miR-124-3p直接靶向ITGB1,双荧光素酶报告基因试验证实了这一点。miR-124-3p的异常表达显著抑制ITGB1 mRNA和蛋白水平,导致致癌特性受损,包括减少胃癌细胞的增殖、迁移和侵袭。此外,ITGB1下调抑制胃癌细胞的生长和侵袭,同时抑制上皮-间质转化(EMT)。值得注意的是,关键的EMT调节因子,如e -钙粘蛋白,被上调。这些发现表明,mir -124-3p介导的ITGB1下调通过抑制细胞增殖、侵袭和转移有效抑制胃癌的进展。结论:miR-124-3p作为肿瘤抑制miRNA,通过靶向ITGB1抑制胃癌的发展。miR-124-3p/ITGB1轴提供了新的见解,可能作为胃癌诊断和治疗的有前途的生物标志物。
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
American journal of translational research
American journal of translational research ONCOLOGY-MEDICINE, RESEARCH & EXPERIMENTAL
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