title: Regulation of DNA methylation on the expression of the FHIT gene contributes to cervical carcinoma cell tumorigenesis.
abstract: The purpose of this study was to determine the effect of the FHIT gene on tumorigenesis of cervical cancer. RT-PCR and MTT were used to detect the expression of FHIT and cell proliferation respectively. Flow cytometry was used to test cell cycle and cell apoptosis. The expression of FHIT was not induced at all four cervical cancer cells treated with demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR). However, a constant level of FHIT expression was detected in the human umbilical vein endothelial cell before and after 5-aza-dC treatment. The proliferation of all four cervical cancer cells was inhibited evidently when treated with 5-aza-dC and the inhibiting rate of cell growth along with the increasing concentration of 5-aza-dC. There was no obvious inhibiting effect on the growth of the human umbilical vein endothelial cell treated with 5-aza-dC. An increasing G1 phase and high apoptosis rate were detected in all four cervical cancer cells. However, a negligible change was seen in the human umbilical vein endothelial cell. These results suggest that aberrant methylation of the FHIT gene might be a key mechanism for silenced FHIT gene, which could be reactivated and whose tumor suppressing function could be restored by demethylating agent treatment.
authors.affiliation: Cancer Biology Research Center, Tongji Hospital, Tongji Medical School, Huazhong University of Science and Technology, Hubei 430030, PR China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Wu
authors.forename: Li
authors.initials: L
authors.lastname: Meng
authors.forename: Hui
authors.initials: H
authors.lastname: Wang
authors.forename: Qian
authors.initials: Q
authors.lastname: Xu
authors.forename: Shixuan
authors.initials: S
authors.lastname: Wang
authors.forename: Sufang
authors.initials: S
authors.lastname: Wu
authors.forename: Ling
authors.initials: L
authors.lastname: Xi
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhao
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Zhou
authors.forename: Gang
authors.initials: G
authors.lastname: Xu
authors.forename: Yuping
authors.initials: Y
authors.lastname: Lu
authors.forename: Ding
authors.initials: D
authors.lastname: Ma
mesh_terms: D017766:Acid Anhydride Hydrolases / Q000235:genetics* / Q000378:metabolism; D017209:Apoptosis; D001374:Azacitidine / Q000031:analogs & derivatives / Q000494:pharmacology; D049109:Cell Proliferation; D002478:Cells, Cultured; D019175:DNA Methylation; D015254:DNA Modification Methylases / Q000037:antagonists & inhibitors; D000077209:Decitabine; D004730:Endothelium, Vascular / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005434:Flow Cytometry; D016193:G1 Phase; D015972:Gene Expression Regulation, Neoplastic; D020868:Gene Silencing; D006801:Humans; D009363:Neoplasm Proteins / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014471:Umbilical Veins / Q000378:metabolism; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000378:metabolism; D000099170:Bis(5'-adenosyl)triphosphatase
chemical_list: D017766:Acid Anhydride Hydrolases; D001374:Azacitidine; D015254:DNA Modification Methylases; D000077209:Decitabine; D004791:Enzyme Inhibitors; D009363:Neoplasm Proteins; D000099170:Bis(5'-adenosyl)triphosphatase