Upregulation of miR-24 promotes cell proliferation by targeting NAIF1 in non-small cell lung cancer

• Published in: Tumor biology 2015-05, Vol.36 (5), p.3693-3701
• Main Authors: Zhao, Guibin, Liu, Lijie, Zhao, Tianshu, Jin, Shoude, Jiang, Sibo, Cao, Shouqiang, Han, Jingquan, Xin, Yanzhong, Dong, Qing, Liu, Xian, Cui, Jian
• Format: Article
• Language: English
• Subjects: Adult; Aged; Animals; Apoptosis Regulatory Proteins - genetics; Biomarkers; Biomedical and Life Sciences; Biomedicine; Cancer Research; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - mortality; Carcinoma, Non-Small-Cell Lung - pathology; Cell growth; Cell Proliferation; Female; Humans; Lung cancer; Lung Neoplasms - genetics; Lung Neoplasms - mortality; Lung Neoplasms - pathology; Male; Mice; MicroRNAs; MicroRNAs - blood; MicroRNAs - physiology; Middle Aged; Nuclear Proteins - genetics; Protein expression; Research Article; Tumorigenesis; Up-Regulation
• ISSN: 1010-4283; 1423-0380
• DOI: 10.1007/s13277-014-3008-4

Recent studies have implied that aberration of miR-24 is linked to various human cancers. However, its role in non-small cell lung cancer (NSCLC) remains obscure. Here, we found that miR-24 was significantly upregulated in NSCLC tissues and patients’ serum. High expression of miR-24 in patients’ serum was independently correlated with a shorter overall survival of NSCLC patients. Depletion of miR-24 inhibited cell proliferation and anchorage-independent survival ability in lung cancer cell lines and reduced tumor formation ability in nude mice. Nuclear apoptosis-inducing factor 1 (NAIF1) was identified to be a functional target of miR-24 in the human lung. Next, we observed that the NAIF1 mRNA expression level in NSCLC tissues was suppressed in comparison to that in adjacent normal tissues. Restoration of NAIF1 in lung cancer cell inhibited cell proliferation and anchorage-independent survival ability, which were found to be similar with those from transfecting a miR-24 inhibitor into lung cancer cells. In conclusion, our study demonstrated that miR-24 was upregulated in NSCLC, and suppressing the expression of miR-24 inhibited tumor characteristics. MiR-24 acted as an oncomir, at least partially through regulation of its functional target NAIF1 in NSCLC. MiR-24 may serve as a novel potential biomarker for NSCLC diagnosis and prognosis.