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

Hyun Min Cho, Hyo Sung Jeon, Soo Young Lee, Kang Jin Jeong, Soon Young Park, Hoi Young Lee, Jung Uee Lee, Ji Hye Kim, Sun Jung Kwon, Eugene Choi, Moon Jun Na, Jaeku Kang, Ji Woong Son

Research output: Contribution to journalArticlepeer-review

56 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)963-967
Number of pages5
JournalExperimental and Therapeutic Medicine
Volume2
Issue number5
DOIs
StatePublished - Sep 2011
Externally publishedYes

Keywords

  • Enhancer of zeste homolog 2
  • Invasion
  • Lung cancer
  • microRNA
  • miR-101

ASJC Scopus subject areas

  • Immunology and Microbiology (miscellaneous)
  • Cancer Research

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