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Effect of CHFR CpG island methylation status on proliferation and apoptosis of esophageal cancer Eca109 cells
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Abstract:
Objective:To study the relationship of CHFR CpG island methylation status on proliferation and apoptosis of esophageal cancer Eca109 cells. Methods: Eca109 cells were treated with different concentrations (2, 5, and 10 μmol/L) of 5-Aza-2′-deoxycytidine (5-Aza-CdR), and untreated Eca109 cells were used as control. Methylation-specific PCR (MSP) analysis was used to evaluate the CpG island methylation status of CHFR gene, and RT-PCR was used to detect the CHFR mRNA expression in Eca109 cells. MTT and flow cytometery were used to determine the proliferation and apoptosis of Eca109 cells treated with different concentrations of 5-Aza-CdR. Results: CHFR CpG island was hypermethylated in the untreated Eca109 cells, and methylated CHFR CpG was demethylated to different degrees in 5-Aza-CdR treatment groups. No expression of CHFR mRNA was found in untreated Eca109 cells, but the relative expression of CHFR mRNA was remarkably increased in 5-Aza-CdR (2, 5, and 10 μmol/L) treatment groups (0.174±0.010, 0.221±0.013, and 0.356±0014). Different concentrations of 5-Aza-CdR inhibited the proliferation (\[30.87±0.74\]%,\[44.60±0.79\]%, and \[56.67±035\]%), and promoted apoptosis of Eca109 cells (\[7.46±1.46\]%, \[16.27±1.61\]%, \[25.29±225\]% vs \[1.83±0.41\]%, P<001). Conclusion: 5-Aza-CdR can partly demethylate CHFR CpG island in esophageal cancer Eca109 cells, inducing CHFR mRNA expression, inhibiting proliferation and promoting apoptosis of Eca109 cells.
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Project Supported:
Project supported by the National Natural Science Foundation of China (No. 30571844), the Science and Technology Development Foundation of Shandong Province (No. 2009GG10002007), and the Natural Science Foundation of Shandong Province (No. ZR2009CM090)
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