MiR-27b suppresses epithelial–mesenchymal transition and chemoresistance in lung cancer by targeting Snail1

• Published in: Life sciences (1973) 2020-08, Vol.254, p.117238-7, Article 117238
• Main Authors: Zhang, Jun, Hua, Xionghuai, Qi, Na, Han, Guangsen, Yu, Juan, Yu, Yongkui, Wei, Xiufeng, Li, Haomiao, Chen, Xiankai, Leng, Changsen, Liu, Qi, Lu, Yingmin, Li, Yin
• Format: Article
• Language: English
• Subjects: Algorithms; Antineoplastic Agents - therapeutic use; Assaying; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - pathology; Cell adhesion & migration; Cell Line, Tumor; Cell migration; Chemoresistance; Cisplatin; Down-Regulation; Drug Resistance, Neoplasm; Epithelial-Mesenchymal Transition - physiology; Flow cytometry; Gene expression; HEK293 Cells; Humans; Lung cancer; Lung Neoplasms - drug therapy; Lung Neoplasms - pathology; Mesenchyme; MicroRNAs; MicroRNAs - physiology; miR-27b; miRNA; Non-small cell lung carcinoma; Small cell lung carcinoma; Snail Family Transcription Factors - physiology; Snail1; Target recognition; Tumors; Western blotting
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2019.117238

MicroRNA-27b (miR-27b) has been shown to play a role in the progression of many different forms of cancer, but its specific relevance in the context of non-small cell lung cancer (NSCLC) remains uncertain. As such, this study sought to explore the role of miR-27b in NSCLC and the mechanisms whereby it functions. We quantified miR-27b and target gene expression via quantitative real-time PCR (RT-qPCR).We then used functional including proliferation assays, migration assay, flow cytometry, and western blotting to explore the mechanisms whereby miR-27b functions in vitro and in vivo. We additionally confirmed miR-27b target genes via luciferase reporter assay. We observed a marked decrease in miR-27b expression in NSCLC patient samples relative to paracancerous control tissues. We further found that altering miR-27b expression levels in vitro affected NSCLC tumor cell migration, proliferation, and ability to undergo epithelial-mesenchymal transition. Through the use of target prediction algorithms we identified Snail to be a miR-27b target protein that was suppressed when this miRNA was highlight expressed. Lastly, we found miR-27b expression to increase NSCLC cell sensitivity to cisplatin through its ability to target Snail. Our results clearly demonstrate that miR-27b can suppress NSCLC tumor development and progression, highlighting this miR-27b/Snail1 axis as putative target for the therapeutic treatment of NSCLC.