miR-96 downregulates RECK to promote growth and motility of non-small cell lung cancer cells

• Published in: Molecular and cellular biochemistry Vol. 390; no. 1-2; pp. 155 - 160
• Main Authors: Guo, Haizhou, Li, Qianping, Li, Weihao, Zheng, Tianliang, Zhao, Song, Liu, Zhangsuo
• Format: Journal Article
• Language: English
• Published: Boston Springer US 01.05.2014; Springer; Springer Nature B.V
• Subjects: B cells; Biochemistry; Biomedical and Life Sciences; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - pathology; Cardiology; Cell adhesion & migration; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation; Cellular biology; Cysteine; Gene Expression Regulation, Neoplastic; GPI-Linked Proteins - biosynthesis; GPI-Linked Proteins - genetics; Growth; Humans; Life Sciences; Lung cancer; Lung cancer, Non-small cell; Lung cancer, Small cell; Medical Biochemistry; MicroRNA; MicroRNAs; MicroRNAs - genetics; Oncology; Proteins; miR-96; Growth; RECK; Migration; Invasion; Non-small cell lung cancer
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-014-1966-x

MicroRNAs play critical roles in the development and progression of non-small cell lung cancer (NSCLC). miR-96 acts as an oncogene in some malignancies, while its role in NSCLC is unclear. Here, we validated that miR-96 was significantly increased in both human NSCLC tissues and cell lines. Inhibition of miR-96 expression remarkably reduced cell proliferation, colony formation, migration, and invasion of NSCLC cells. Reversion-inducing-cysteine-rich protein with kazal motifs (RECK) was identified as a target of miR-96 in NSCLC cells. In addition, the expression of RECK was found to be negatively correlated with the expression of miR-96 in NSCLC tissues. Our data suggest that miR-96 might promote the growth and motility of NSCLC cells partially by targeting RECK.