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WU Ying, WANG Shi-xuan, MA Ding. Pattern of FHIT Gene 5'CpG Island Methylation Contribute to Human Cervical Carcinoma Cell Tumorigenesis[J]. Cancer Research on Prevention and Treatment, 2007, 34(08): 557-559. DOI: 10.3971/j.issn.1000-8578.181
Citation: WU Ying, WANG Shi-xuan, MA Ding. Pattern of FHIT Gene 5'CpG Island Methylation Contribute to Human Cervical Carcinoma Cell Tumorigenesis[J]. Cancer Research on Prevention and Treatment, 2007, 34(08): 557-559. DOI: 10.3971/j.issn.1000-8578.181

Pattern of FHIT Gene 5'CpG Island Methylation Contribute to Human Cervical Carcinoma Cell Tumorigenesis

  • Objective  To determine whether hypermethylation of FHIT played an important role in cervical tumorigenesis. Methods  By incubating DNA in the presence of a methylase, we investigated the methylation of FHIT in four cervical cancer cell lines and one human umbilical vein endothelial cell line treating with the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (5-aza-dC) . The expression of FHIT was also monitored by RT-PCR and immunofluorescence technique before and af ter 5-aza-dC treatment . Results  We found that methylation of FHIT occured in the four cervical cancer cell lines instead of the ECV-304. Through RT-PCR and immunofluorescence technique, we found that the expression of FHIT, which could hardly be detected in all four cervical cancer cells, was significant different af ter 5-aza-dC treatment . However, the ECV-304 cell expressed FHIT at constant levels before and af ter 5-aza-dC t reatment . Conclusion  We concluded that hypermethylation of FHIT gene occurred f requently in cervical tumorigenesis. And hypermethylation within the regulatory sequences of FHIT gene might be an important means for its inactivation in cervical cancer.
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