MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

Thoracic Cancer

Yajiao Sun¹  JingWen Zhang¹  FuHui Chen¹  Zhe Jiang¹ 

[1] Department of Pulmonary and Critical Care Medicine The Second Affiliated Hospital of Harbin Medical University Heilongjiang China;

关键词: ALCAM;    miR‐148b;    NF‐κB;    NSCLC;    progression;   

DOI  :  10.1111/1759-7714.13285

来源: DOAJ

【 摘 要 】

Background Non‐small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. MiRNAs are recognized as important molecules in cancer biology. The aim of the study was to identify a novel biomarker miR‐148b and its mechanism in the modulation of NSCLC progression. Methods The expressional level of miR‐148b was analyzed by RT‐PCR. The effect of miR‐4317 on proliferation was evaluated through 3‐(4,5‐Dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2Htetrazolium bromide (MTT) assay. The effect of miR‐148b on the metastasis of NSCLC was detected through transwell assays. The verification of the target of miR‐148b was assessed by TargetScan and dual‐luciferase reporter assay. The related proteins in this study were analyzed by western blot. Results Our findings confirmed that miR‐148b was decreased in NSCLC and NSCLC patients with lower expression exhibited poorer overall survival (OS). Increasing miR‐148b significantly repressed proliferation, invasion and migration. More importantly, activated leukocyte cell adhesion molecule (ALCAM) was determined as the direct target of miR‐148b, and reintroduction of ALCAM attenuated miR‐148b effect on the progress of NSCLC. In addition, NF‐κB signaling pathway was modulated by miR‐148b/ALCAM axis. Conclusions Our results indicated that miR‐148b is able to suppress NSCLC growth and metastasis via targeting ALCAM through the NF‐κB pathway. These findings provided new evidence that miR‐148b serves as a potential biomarker and novel target for NSCLC treatment.

【 授权许可】

Unknown