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首页> 外文期刊>Medical science monitor : >MicroRNA-140 Inhibits Cell Proliferation in Gastric Cancer Cell Line HGC-27 by Suppressing SOX4
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MicroRNA-140 Inhibits Cell Proliferation in Gastric Cancer Cell Line HGC-27 by Suppressing SOX4

机译:MicroRNA-140通过抑制SOX4抑制胃癌细胞HGC-27的细胞增殖

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摘要

BACKGROUND Gastric cancer is a malignant tumor with a high morbidity and mortality. MicroRNAs are important regulators of gene expression, influencing the progression of gastric cancer. This study aimed to reveal the role of microRNA-140 (miR-140) in gastric cancer cell proliferation and its potential mechanisms. MATERIAL AND METHODS Gastric cancer tissues and cell lines BGC-823, SGC-7901, and HGC-27 were used to analyze miR-140 levels compared to normal tissues and cell line GES-1. In HGC-27 cells transfected with miR-140 mimic, we performed MTT, colony formation assay, and cell cycle assay by flow cytometry. SOX4, a predicted target of miR-140, was mutated to verify its regulation by miR-140, and was overexpressed to analyze its function in cell proliferation. Doxorubicin treatment was performed to investigate the effect of miR-140 on drug resistance. RESULTS miR-140 was down-regulated in gastric cancer tissues and cell lines, with the lowest expression level in HGC-27. miR-140 overexpression inhibited HGC-27 cell viability and colony formation and resulted in G0/G1 arrest. miR-140 suppressed SOX4 expression via binding to the 3’ untranslated region, while the mutant SOX4 could not be regulated. Overexpressing SOX4 led to promoted cell viability, colony formation, and cell cycle progress. miR-140 overexpression also improved the anti-viability effects of doxorubicin, suggesting its potential in reducing the drug resistance of gastric cells. CONCLUSIONS These findings suggest that miR-140 directly inhibits SOX4, which might be one of its mechanisms in suppressing gastric cancer cell proliferation. This study provides a promising therapeutic strategy for treating gastric cancer and facilitates microRNA research in various diseases.
机译:背景技术胃癌是具有高发病率和死亡率的恶性肿瘤。 MicroRNA是基因表达的重要调节剂,影响胃癌的进展。这项研究旨在揭示microRNA-140(miR-140)在胃癌细胞增殖中的作用及其潜在机制。材料与方法胃癌组织和细胞系BGC-823,SGC-7901和HGC-27用于分析与正常组织和细胞系GES-1相比的miR-140水平。在用miR-140模拟物转染的HGC-27细胞中,我们通过流式细胞术进行了MTT,集落形成测定和细胞周期测定。 SOX4是miR-140的预期靶标,被突变以验证其对miR-140的调控,并被过表达以分析其在细胞增殖中的功能。进行阿霉素治疗以研究miR-140对耐药性的影响。结果miR-140在胃癌组织和细胞系中表达下调,在HGC-27中最低。 miR-140过表达抑制HGC-27细胞活力和集落形成,并导致G0 / G1阻滞。 miR-140通过与3'非翻译区结合而抑制了SOX4的表达,而突变型SOX4则无法调控。过表达SOX4导致细胞活力增强,集落形成和细胞周期进程。 miR-140的过表达还改善了阿霉素的抗生存能力,表明其在降低胃细胞耐药性方面具有潜力。结论这些发现表明miR-140直接抑制SOX4,这可能是其抑制胃癌细胞增殖的机制之一。这项研究为胃癌的治疗提供了一种有希望的治疗策略,并促进了各种疾病中microRNA的研究。

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