癌症研究
癌基因
癌变
细胞凋亡
胆囊癌
癌症
TLR4型
生物
NF-κB
Toll样受体
分子医学
信号转导
转移
细胞周期
核受体
受体
内科学
医学
细胞生物学
先天免疫系统
转录因子
基因
生物化学
作者
Bo Ouyang,Ningfeng Pan,Haifeng Zhang,Chuanming Xing,Wu Ji
摘要
Gallbladder cancer (GBC) is a carcinoma of the biliary tract, which is common in developing countries and is associated with a high fatality rate. The aim of the present study was to investigate the mechanisms underlying the occurrence and development of GBC. A decrease in the expression of miR‑146b‑5p and an increase in the expression of its target gene Toll‑like receptor 4 (TLR4) were first observed in GBC tissues. Further study demonstrated that an increase in TLR4 expression caused by a decrease in miR‑146b‑5p expression led to activation of nuclear factor (NF)‑κB signaling. GBC cells were cultured in vitro, and it was observed that overexpression of miR‑146b‑5p effectively inhibited their viability, proliferation, migration and invasion, and increased their apoptosis. Using a BALB/c nude mouse xenograft model, it was demonstrated that overexpression of miR‑146b‑5p was sufficient to reduce tumor volume and alleviate pathological characteristics. Overall, the results of the present study indicated that the decrease in the expression of miR‑146b‑5p increased TLR4 expression and indirectly activated the NF‑κB signaling pathway, thereby regulating the development of GBC.
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