Methylation Of MiR-200c Promoter Region Is Associated With Resistance To EGFR-TKI In Lung Cancer Cells

Objective:1. To investigate the effect of growth ihhibition rates on human non-small cell lung cancer (NSCLC) cell lines.2. To study differently expression of miR-200c of NSCLC cell lines. And to examine the relationship between the response to EGFR-TKI and the expression of miR-200c of NSCLC cell lines.Methods:NSCLC cell lines H1650, HCC827with EGFR19deletion and cell lines H358, H1299with wild type EGFR were used in this study. The response to gefitinib was examed by Cell counting Kit-8(CCK-8) assay.The expression of miR-200c was examed by RT-PCR analysis.Results:The cell lines HCC827and H358were sensitive to gefitinib and highexpressed miR-200c. The cell lines H1650and H1299were insensitive to gefitinib and lack of miR-200c expression.Conclusion:The response of NSCLC cell lines to gefitinib may be positively correlated with the expression of miR-200c. Objective:To examine the relationship between the response to EGFR-TKI in NSCLC cell lines and miR-200c promoter methylation.Methods:NSCLC cell lines H1650, HCC827,H358and H1299were used in this study. The methylation of miR-200c promoter region was examed by methylation-specific PCR (MSP).5-aza-CdR was used to treat the four cell lines and the response to gefitinib and the expression of miR-200c was observed.Results:The cell lines HCC827and H358with miR-200c promoter unmethylation were sensitive to gefitinib.The cell lines H1650and H1299with miR-200c promoter methylation were insensitive to gefitinib. When5-aza-CdR was used to treat the cell lines, H1650and H1299expressed higher miR-200c and were more sensitive to gefitinib than before(P<0.05). HCC827and H358treated by5-aza-CdR had no alteration of the expression and the sensibility to gefitinib(P>0.05).Conclusion:The expression of miR-200c in NSCLC cell lines are up-regulated by DNA methylation inhibitor5-aza-CdR, which increases the sensitivity to gefitinib.