miR-34c-3p通过抑制巨噬细胞M2极化抑制鼻咽癌的发展。

Yu Zi Ji, Yu Jie Wang, Ji Qing Ma, Zhi Hua Yin, Fei Liu, Yan Zi Zang, Guang Ke Wang, Yong Tai
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引用次数: 0

摘要

目的:miR-34c-3p在鼻咽癌(NPC)中表达下调。miR-34c-3p在鼻咽癌中的生物学作用及其潜在机制尚不清楚,本研究对其进行了探讨。方法:采用流式细胞术和免疫组织化学染色法检测分化簇86 (CD86)和分化簇206 (CD206)的表达;采用实时定量聚合酶链反应(qRT-PCR)和western blotting检测mRNA表达和蛋白水平;采用细胞计数试剂盒-8 (CCK8)和transwell法评估细胞增殖、迁移和侵袭;采用苏木精-伊红(HE)染色评价肿瘤组织病理变化。结果:我们的研究结果显示miR-34c-3p mimic通过靶向SLC7A11显著抑制巨噬细胞的M2极化,转染miR-34c-3p mimic的M2巨噬细胞抑制鼻咽癌细胞的增殖、迁移和侵袭。体内实验进一步证实miR-34c-3p模拟物阻断肿瘤生长,减少肿瘤组织炎症浸润。结论:本研究对鼻咽癌的发病机制和治疗策略提供了新的认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-34c-3p Inhibits Nasopharyngeal Carcinoma Development via Inhibiting M2 Polarization of Macrophages.

Objective: miR-34c-3p is down-regulated in nasopharyngeal carcinoma (NPC). The biological role of miR-34c-3p in NPC and its underlying mechanisms are unknown and were explored in this study.

Methods: Flow cytometry and immunohistochemical staining were employed to detect cluster of differentiation 86 (CD86) and cluster of differentiation 206 (CD206) expression; quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were employed to examine mRNA expression and protein levels; cell counting kit-8 (CCK8) and transwell assays were employed to assess cell proliferation, migration, and invasion; and hematoxylin-eosin (HE) staining was employed to assess pathological changes in tumor tissues.

Results: Our results revealed that the miR-34c-3p mimic markedly inhibited M2 polarization of macrophages by targeting SLC7A11, and M2 macrophages transfected with the miR-34c-3p mimic inhibited the proliferation, migration, and invasion of NPC cells. The in vivo experiments further confirmed that miR-34c-3p mimics blocked tumor growth and reduced inflammatory infiltration in tumor tissues.

Conclusion: This study provides novel insights into the pathogenesis of NPC and a new treatment strategy.

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