microRNA-101 inhibits lung cancer invasion through the regulation of enhancer of zeste homolog 2

• Published in: Experimental and therapeutic medicine Vol. 2; no. 5; pp. 963 - 967
• Main Authors: CHO, HYUN MIN, JEON, HYO SUNG, LEE, SOO YOUNG, JEONG, KANG JIN, PARK, SOON-YOUNG, LEE, HOI YOUNG, LEE, JUNG UEE, KIM, JI HYE, KWON, SUN JUNG, CHOI, EUGENE, NA, MOON JUN, KANG, JAEKU, SON, JI WOONG
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.09.2011
• Subjects: enhancer of zeste homolog 2; invasion; lung cancer; microRNA; miR-101
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2011.284

microRNAs (miRNAs) may function as oncogenes or tumor-suppressor genes depending on the targets that are regulated. Enhancer of zeste homolog 2 (EZH2) is the target of miR-101 and a member of the polycomb repressive complex 2, which is involved in the methylation of histone H3 at lysine 27 (H3K27). Therefore, we aimed to ascertain whether or not the overexpression of miR-101 inhibits invasion of lung cancer through regulation of EZH2. In this study, the expression of miR-101 was down-regulated and the expression of EZH2 was up-regulated in lung cancer. Global methylation of H3K27 was higher in metastatic lung cancer than in early lung cancer lesions. Overexpression of miR-101 induced a marked reduction in EZH2 mRNA levels in several lung cancer cell lines. A reduction in the trimethyl H3K27 histone mark was detected at the CDH1 promoter in miR-101 precursor-transfected cells. Moreover, the expression of CDH1 and MMP-2 was reversed by miR-101 transfection. Therefore, the overexpression of miR-101 inhibits the invasiveness of lung cancer. miR-101 may be a potent tumor suppressor by altering chromatin structure through repression of EZH2 and may be a potential therapeutic tool for patients with lung cancer.