The Role of Epigenetics in Cervical Cancer

Cervical cancer is the fourth most common type of cancer among women worldwide resulting in 528,475 new cases and 268,224 deaths. The principal etiological factor of cervical cancer is the persistent infection with high-risk types of human papillomaviruses (HPV), however is not sufficient, other factors like age, smoking, oral contraceptives, and genetic background are implicated in the development of this neoplasia. Although the understanding of cervical carcinogenesis has been increasing in recent decades, the epigenetic modifications (DNA methylation, histone modification, miRNAs and long non-coding RNAs) and its contribution to the development of cervical cancer remain largely unknown. In the next chapter, we will recapitulate the described findings on the alteration of epigenetic factors that, together with the persistent infection of HPV, could contribute to the malignant and invasive phenotype in cervical cancer

The roles of histone post-translational modifications in the formation and function of a mitotic chromosome

During mitosis, many cellular structures are organized to segregate the replicated genome to the daughter cells. Chromatin is condensed to shape a mitotic chromosome. A multiprotein complex known as kinetochore is organized on a specific region of each chromosome, the centromere, which is defined by the presence of a histone H3 variant called CENP-A. The cytoskeleton is re-arranged to give rise to the mitotic spindle that binds to kinetochores and leads to the movement of chromosomes. How chromatin regulates different activities during mitosis is not well known. The role of histone post-translational modifications (HPTMs) in mitosis has been recently revealed. Specific HPTMs participate in local compaction during chromosome condensation. On the other hand, HPTMs are involved in CENP-A incorporation in the centromere region, an essential activity to maintain centromere identity. HPTMs also participate in the formation of regulatory protein complexes, such as the chromosomal passenger complex (CPC) and the spindle assembly checkpoint (SAC). Finally, we discuss how HPTMs can be modified by environmental factors and the possible consequences on chromosome segregation and genome stability