Source: Annual Congress 2010 - Pathology of lung cancer

Abstract

Background: Some microRNAs (miRNAs) are aberrantly expressed in human cancers, suggesting their function as either oncogenes or tumor suppressor genes. According to miRNA profiles on microarray, miR-101 was down-expression in lung cancer. EZH2 (Enhancer of zeste homolog 2) is predicted target of miR-101 through three public algorithms and a member of the polycomb repressive complex 2 which involves methylation of Histone H3 at lysine 27.
Objectives: To confirm the hypothesis that the miR-101 has a role of inhibitor on cell growth and invasion in lung cancer.
Methods: We measured expression of miR-101 and EZH2 using quantitative reverse transcription PCR (qRT-PCR) in lung cancer. To examine whether miR-101 could regulate EZH2 in lung cancer, we performed transient transfection of miR-101 into lung cancer cell line and then measured expression of EZH2.
Results: miR-101 was down-regulated and EZH2 was up-regulated in lung cancer. Over-expression of miR-101 induced marked reduction of EZH2 mRNA levels in lung cancer cell line A549, H522, H1438. We found reduction of the tri-methyl H3K27 histone mark at the CDH1 promoter in miR-101 precursor transfected cell, this gene is known as EZH2 target genes. The cell invasion and growth rates decreased in miR-101 precursor treated cells.
Conclusion: Abnormal down-regulation of miR-101 could lead to the over-expression of EZH2 in lung cancer. miR-101 may be a potent tumor suppressor by altering chromatin structure through repression of EZH2 and might to be potential candidate therapeutic tool in lung cancer.

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M. J. Na, S. J. Kwon, E. Choi, J. K. Kang, S. K. Kim, S. Y. Lee, S. Y. Park, J. U. Lee, Y. J. Kim, J. W. Son (Daejeon, Republic Of Korea). MicroRNA-101 inhibits lung cancer growth and invasion through regulation of EZH2. Eur Respir J 2010; 36: Suppl. 54, 3259

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