Abstract

Objective To investigate the effect of 5-aza-2'deoxycytidine (5-Aza-CdR) on proliferation and expression of RASSF1 A gene in human ovarian cancer cell line SKOV3 and 3AO.Methods SKOV3 and 3AO cells were treated with different concentrations (0.5,5,50 μmol/L) of DNA methyltransferase inhibitor 5-Aza-CdR.RT-PCR and Western Blot were adopted to detect expression of mRNA and protein of RASSF1A gene before and after treatment with 5-Aza-CdR respectively.Results Compared with control group,when the 5-Aza-CdR concentration was 0.5,5,50 μmol/L after drug treatment,human ovarian cancer cells could significantly inhibit tumor cell growth; SKOV3 and 3AO cells in control group were observed weaker expression of RASSF1A mRNA.After treated with 5-Aza-CdR,the expressions of RASSF1A mRNA were observed increased with the increase of the drug concentration.After treated with different concentration of 5-Aza-CdR,the expressions of RASSF1A mRNA treated with 0.5 μmol/L 5-Aza-cdR was lower than those treated with 5 and 50 μmol/L 5-Aza-cdR (t =-8.866,P =0.01 ; t =-12.256,P =0.000).However,expressions of RASSF1A mRNA treated with 5 and 50 μmol/L 5-Aza-cdR respectively showed no statistical significance (t =0.431,P =0.689).Expressions of RASSF1A protein treated with 0.5 μmol/L 5-Aza-cdR and 5 μmol/L 5-Aza-cdR didn't show statistically significant (t =-1.586,P =0.188).Conclusion Expressions of RASSF1A mRNA and protein in SKOV3 and 3AO cells were evidently enhanced.As one kind of methyltransferases inhibitors,5-Aza-CdR can inhibit ovarian cancer cell line SKOV3,3AO growth through the RASSF1A promoter methylation,and thus promote their apoptosis. Key words: Ovarian neoplasms; RASSF1A gene; 5-aza-2'deoxycytidine

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.