How to cite item

MicroRNA-1304 suppresses human non-small cell lung cancer cell growth in vitro by targeting heme oxygenase-1

  
@article{APS9517,
	author = {Cheng-gang LI and Meng-fan PU and Chun-zhu LI and Man GAO and Ming-xia LIU and Cun-zhi YU and Hong YAN and Chun PENG and Yang ZHAO and Yu LI and Ze-long MA and Xin-ming QI and Yi-zheng WANG and Ling-ling MIAO and Jin REN},
	title = {MicroRNA-1304 suppresses human non-small cell lung cancer cell growth  in vitro  by targeting heme oxygenase-1},
	journal = {Acta Pharmacologica Sinica},
	volume = {38},
	number = {1},
	year = {2017},
	keywords = {},
	abstract = {Previous studies have shown that microRNA-1304 (miR-1304) is dysregulated in certain types of cancers, including non-small cell lung cancer (NSCLC), and might be involved in tumor survival and/or growth. In this study we investigated the direct target of miR-1304 and its function in NSCLC in vitro. Human lung adenocarcinoma cell lines (A549 and NCI-H1975) were studied. The cell proliferation and survival were investigated via cell counting, MTT and colony-formation assays. Cell apoptosis and cell cycle were examined using annexin V-PE/7-AAD and PI staining assays, respectively. The dual-luciferase reporter assay was used to verify post-transcriptional regulation of heme oxygenase-1 (HO-1) by miR-1304. CRISPR/Cas9 was used to deplete endogenous miR-1304. Overexpression of MiR-1304 significantly decreased the number and viability of NSCLC cells and colony formation, and induced cell apoptosis and G0/ G1 phase cell cycle arrest. HO-1 was demonstrated to be a direct target of miR-1304 in NSCLC cells. Restoration of HO-1 expression by hemin (20 μmol/L) abolished the inhibition of miR-1304 on cell growth and rescued miR-1304-induced apoptosis in A549 cells. Suppression of endogenous miR-1304 with anti-1304 significantly increased HO-1 expression and promoted cell growth and survival in A549 cells. In 17 human NSCLC tissue samples, miR-1304 expression was significantly decreased, while HO-1 expression was significantly increased as compared to normal lung tissues. MicroRNA-1304 is a tumor suppressor and HO-1 is its direct target in NSCLC. The results suggest the potential for miR-1304 as a therapeutic target for NSCLC.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/9517}
}