Am J Physiol Regul Integr Comp Physiol 2008, 294:R1117–1129.PubMedCrossRef 77. Saarni SE, Rissanen A, Sarna S, Koskenvuo M, Kaprio J: Weight cycling of athletes and subsequent weight gain in middleage. Int J Obes 2006, 30:1639–1644.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions

ETT conceived of the review topic and drafted the manuscript. AES conceived, drafted and revised the manuscript. LEN helped to draft and revise the manuscript. All see more authors read and approved the final manuscript.”
“Background Cervical cancer is the second most common cancer in women worldwide and the leading cause of cancer SN-38 manufacturer deaths in women in developing countries. It is obviously that many genetic and epigenetic alternations occur during cervical tumorigenesis. Among those changes, aberrant promoter methylation of tumor-suppressor genes gives rise to its silencing functions and results in the significant carcinogenesis

of cervical cancer. Currently, the known repressor genes are related to cervical cancer including CCNA1, CHFR, FHIT, PAX1, PTEN, SFRP4, TSLC1 and etc [1]. All these genes mentioned above have performed a wide variety of functions to regulate the transcription and expression, any of which down-regulation as well as promoter hypermethylation will lead to the precursor lesions in cervical

development and malignant transformation. DNA methylation is catalyzed by several DNA methyltransferases, 3-oxoacyl-(acyl-carrier-protein) reductase including DNMT1, DNMT3a, DNMT3b and etc. DNMT1 is responsible for precise duplicating and maintaining the buy A-769662 pre-existing DNA methylation patterns after replication. As reported by Szyf [2], DNMT1 inhibited the transcription of tumor suppressor genes and facilitated the formation of tumorigenesis, which linked to the development of cervical cancer. Meanwhile, Inhibition of DNMT1 activity could reduce hypermethylation of repressive genes and promote its re-expression, and reverse phenotype of malignant tumor. Thus, specific inhibition of DNMT1 could be one strategy for cervical therapy. In our study, we detected the demethylation and re-expression levels of seven cervical cancer suppressor genes with DNMT1 silencing in Hela and Siha cells. The aim was to elucidate the relations between DNMT1 and abnormal methylation of these genes’ promoter as well as the malignant phenotype of tumor cells, which might contribute to the investigations of functions and regulation roles of DNMT1 in cervical cancer. Materials and methods Cell culture and transfection The Hela and Siha human cervical cancer cells lines were obtained from American Type Culture Collection (Manassas, VA, USA). Lipofectamine TM2000 was purchased from Invitrogen Co.