G9a-KD cells showed significantly increased chromosome numbers than the SUV-KD cells and FH1 control cells. This was true regardless of the cell line types used. Both stable G9a-KD clones of the breast cancer cell line MCF7 and the lung cancer cell line H1299 also showed an increased number of chromosomes compared to control cells. Centrosomes are essential for proper cellular polarity and balanced distribution of chromosomes. We used an antibody against c-tubulin to evaluate the centrosomes in the KD cells. Although the majority of the cells in both control and G9a-KD showed normal centrosome numbers, we detected centrosome amplification in about 25% of the cells in the G9aKD cells. This was not detected in the control cells and SUV-KD cells. Centrosome abnormality was also observed in both MCF7-G9a-KD cells and H1299-G9a-KD cells in around 20% of the cells. Thus, G9a might play a critical role in regulating centrosome duplication, presumably through chromatin structure rather than by affecting gene expression in cancer cells. The chromatin structure at telomeres is also important to maintain the length of telomere repeats. We investigated telomere function in the G9a-KD and the SUV-KD cells. First, we used telo-FISH assay to evaluate telomere length. Significant reduction in the telomere Isosorbide signal intensity was observed in the G9aKD and SUV-KD treated PC3 cells, as compared to the control cells suggesting that regulation of telomere length was disrupted in these KD cells. A representative example of the decrease in the telomere signal is shown in figure 4A. We next quantified telomerase activity in those cells by the TRAP assay and found reduction of telomerase activity in the G9a-KD cell line. Therefore, the shortened telomere length in the G9a-KD cells might be the result of altered telomerase activity. The decreased level of hTERT expression in the G9a-KD cells lends support to these findings. In contrast, the SUV-KD cells showed similar levels of telomerase activity to the control cells, indicating that telomere dysfunction in the SUV-KD cells might depend on mechanisms other than hTERT expression, probably due to alterations of H3K9 methylation status at telomeric heterochromatin.