| For the better part of the last century, physicians and research scientists have steadfastly postulated that irreversible genomic mutations were the primary causes of cancer. However, recent ground-breaking research in the field of epigenetics revealed that many types of cancers are also caused by epigenetic changes. In contrast to DNA mutations, epigenetic changes are reversible and drug therapies targeting them may be more individualized and potentially less toxic to patients. Therefore, a greater understanding of epigenetic mechanisms would provide improved cancer drug strategies.;Posttranslational histone modifications, particularly methylation, modulate chromatin structure to regulate cellular growth, differentiation and apoptosis. Aberration of these processes can lead to carcinogenesis. Once considered irreversible, histone methylation and the newly discovered enzymes responsible for their removal, the histone demethylases, have opened an unexplored area of epigenetics and cancer research. Here, we identify JMJD5 (now renamed KDM7), a novel uncharacterized JmjC family member, as a new histone demethylase that demethylates coding region associated H3K36me2 resulting in increased transcription of specific cell cycle regulatory genes and cell cycle progression. Furthermore, KDM7 is overexpressed in multiple cancer types, including malignant breast tumors. Loss-of-function studies in breast cancer cells resulted in cell cycle arrest, indicating its importance in breast cancer cell proliferation. Additionally, I show that JMJD5/KDM7 may differentially regulate other cell cycle genes. Ultimately, the understanding of the mechanics behind KDM7 mediated epigenetic control of gene expression may provide a promising new target for cancer drug development. |
