分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

miR-143-3p shuttled by M2 macrophage-derived extracellular vesicles induces progression of colorectal cancer through a ZC3H12A/C/EBPβ axis-dependent mechanism

Wenli Zhou, Shiquan Li, Xiaona Zhang, Chao Li, Jiantao Zhang

Journal:INTERNATIONAL IMMUNOPHARMACOLOGY

IF:5.6

DOI:10.1016/j.intimp.2023.110137

PMID:37126984

Published:2023-04-29

research field:肿瘤学分子生物学细胞生物学免疫学

Abstract

Extracellular vesicles (EVs) exhibit pivotal functions in cancer via intercellular communication through shuttling microRNA (miRNA) and protein. Therefore, we aim to elucidate the function of EVs containing miR-143-3p derived from M2 macrophages in colorectal cancer (CRC). EVs derived from M2 macrophages were isolated and characterized. Expression changes in miR-143-3p were calculated in the EVs. The effects of M2 macrophage-derived EV carrying miR-143-3p on cell biological processes and in vivo tumorigenic ability concerning ZC3H12A were examined. EVs derived from M2 macrophages could stimulate the aggressive tumor biology of CRC cells. Meanwhile, in vivo results showed that M2 macrophage-derived EVs facilitated tumor growth and epithelial-mesenchymal transition. M2 macrophage-secreted EVs could transfer miR-143-3p to CRC cells, in which miR-143-3p bound to the 3′UTR of ZC3H12A and inhibited its expression, leading to elevation of the expression of transcription factor C/EBPβ. Overall, M2 macrophage-derived EV miR-143-3p inhibits ZC3H12A gene and increases C/EBPβ expression to facilitate the development of CRC, which provides novel targets for the molecular treatment of CRC.

本文使用的Yeasen产品

购物车
客服
转染试用