These results suggest that 1Me, 2Me, or 3Me at K9H3 occupy distinct chromosome domains and each of the three states of H3K9 methylation plays a unique role in the structural and functional organization of chromosomes. Regulation of higher-order chromosome structure affects mitotic fidelity and ensures balanced chromosome segregation. Heterochromatin assembly at centromeres facilitates both kinetochore formation and sister chromatid cohesion. Furthermore, the formation of chromatin structures at telomeres also serves to maintain the length of telomere repeats. Studies in fission yeast showed that interaction between 3MeH3K9 and Swi6/HP1 is required for chromosome segregation in mitosis. In mammals, mitotic chromosomes Dimaprit dihydrochloride display enriched 2MeH3K9 at centromeric regions and pronounced 3MeH3K9 at pericentric heterochromatin. Knockout of Suv39h1 and Suv39h2 in mouse results in widespread genomic instability and increased incidence of lymphomas, suggesting that 3MeH3K9 is a critical modification to maintain chromosomal environments. 2MeH3K9 has also been implicated in DNA-methylation associated gene silencing, but the enzyme control of this event has not been defined. Cancer cells are characterized by prominent epigenetic dysregulation, including altered chromatin modification. Previously we found increased level of G9a in human cancers, although the functional role of the HMTs overexpression in cancer remains unclear. Here, we show that knockdown of G9a and SUV39H1 in cancer cells remarkably inhibited cell growth and led to morphologically senescent cells with telomere abnormalities. We found that G9a KD but not SUV39H1 KD induces extensive chromosome instability and centrosome disruption. These data suggest that G9a as well as SUV39H1 are required to maintain the malignant phenotype and could be valid therapeutic targets in human neoplasia. None of the patients received thrombolytic Olsalazine Disodium therapy, since it was not available in our centre during the study period.