Cervical cancer (CC) is one of the most malignant tumors and the second or third 
most common type of cancer in women worldwide. The association between human 
papillomavirus (HPV) and CC is widely known and accepted (99.7% of cases). At 
present, the pathogenesis mechanisms of CC are not entirely clear. It has been 
shown that inactivation of tumor suppressor genes and activation of oncogenes 
play a significant role in carcinogenesis, caused by the genetic and epigenetic 
alterations. In the past, it was generally thought that genetic mutation was a 
key event of tumor pathogenesis, especially somatic mutation of tumor suppressor 
genes. With deeper understanding of tumors in recent years, increasing evidence 
has shown that epigenetic silencing of those genes, as a result of aberrant 
hypermethylation of CpG islands in promoters and histone modification, is 
essential to carcinogenesis and metastasis. The term epigenetics refers to 
heritable changes in gene expression caused by regulation mechanisms, other than 
changes in DNA sequence. Specific epigenetic processes include DNA methylation, 
chromotin remodeling, histone modification, and microRNA regulations. These 
alterations, in combination or individually, make it possible to establish the 
methylation profiles, histone modification maps, and expression profiles 
characteristic of this pathology, which become useful tools for screening, early 
detection, or prognostic markers in cervical cancer. This paper reviews recent 
epigenetics research progress in the CC study, and tries to depict the 
relationships between CC and DNA methylation, histone modification, as well as 
microRNA regulations.