Koul et al. BMC Cancer 2010, 10:328 http://www.biomedcentral.com/1471-2407/10/328 Page 5 of 8 Figure 4 Iripallidal effects expression of cell cycle regulators and DNA damage repair response molecules. Representative blot is shown from three independent experiments with identical results. C and I denote control and Iripallidal, respectively. Western blot analysis reveals (a) increase in p21, p27 and decrease in cyclin D1, cMyc levels (b) increase in gH2AX in A172, LN229, T98G and U87MG glioma cells treated with 20 μM Iripallidal, as compared to control. Figures (a) and (b) are representative blot shown from three independent experiments with identical results. Blots were reprobed for b-actin to establish equivalent loading. Figure 5 Iripallidal decreases hTERT activity and colony forming ability of glioma cells. (a) Glioma cells were treated with 20 μM Iripallidal and TeloTAGGG Telomerase PCR ELISA was performed. A decrease in hTERT activity was observed in Iripallidal treated cells as compared to control. (b) Iripallidal decreases the ability of glioma cells to form colonies in soft agar. Soft agar assay was performed on cells that were left untreated or treated with Iripallidal for 6 days. The graph indicates the percentage of colonies formed. Values in (a) and (b) represent the means ± SEM from 3 individual experiments. * Significant decrease from control (P < 0.05). compared to their respective controls (Fig. 6a). These findings indicate that Iripallidal not only inhibits prolif- eration of GBM, but also exhibits anti-proliferative activity against a wide variety of human cancers. To show the selectivity of Iripallidal for tumor cells, the effect of Iripallidal was investigated on normal human monocytes. Treatment of monocytes with Iripallidal induced ~8-10% decrease in viability, suggesting that the anti-proliferative ability of Iripallidal is selective for transformed cells (Fig. 6b).