Dracorhodin perchlorate suppresses proliferation and induces apoptosis in human prostate cancer cell line PC-3

Abstract

The growth inhibition and pro-apoptosis effects of dracorhodin perchlorate on human prostate cancer PC-3 cell line were examined. After administration of 10-80 μmol/L dracorhodin perchlorate for 12-48 h, cell viability of PC-3 cells was measured by MTT colorimetry. Cell proliferation ability was detected by colony formation assay. Cellular apoptosis was inspected by acridine orange-ethidium bromide fluorescent staining, Hoechst 33258 fluorescent staining, and flow cytometry (FCM) with annexin V-FITC/propidium iodide dual staining. The results showed that dracorhodin perchlorate inhibited the growth of PC-3 in a dose- and time-dependent manner. IC50 of dracorhodin perchlorate on PC-3 cells at 24 h was 40.18 μmol/L. Cell clone formation rate was decreased by 86% after treatment with 20 μmol/L of dracorhodin perchlorate. Some cells presented the characteristic apoptotic changes. The cellular apoptotic rates induced by 10-40 μmol/L dracorhodin perchlorate for 24 h were 8.43% to 47.71% respectively. It was concluded that dracorhodin perchlorate significantly inhibited the growth of PC-3 cells by suppressing proliferation and inducing apoptosis of the cells.

Dracorhodin perchlorate induces apoptosis in bladder cancer cells through Bcl-2, Bcl-XL, survivin down-regulation and caspase-3 activation

“…The rates of depletion of mitochondrial membrane potential were 82.4 ± 2.4% 71.7 ± 1.9%, and 61.0 ± 1.6% in cells treated with 100 µM of dracorhodin perchlorate for 12, 24, and 48 h respectively as compared to 95.9 ± 0.4% in control group (Figure 4). Our data corroborate with the previously reported results that dracorhodin Perchlorate induced dissipation of mitochondrial membrane potential, which provide the evidence for direct contribution of mitochondria in the dracorhodin perchlorateinduced apoptosis (He et al, 2011;Rasul et al, 2012a;Xia et al, 2005;Xia et al, 2006).…”

“…The results of flow cytometric analysis showed that the rates of apoptosis were 15.5 ± 2.2%, 24.4 ± 2.1% and 45.5 ± 1.8% in the cells treated with 100 µM of dracorhodin perchlorate for 12, 24, and 48 h respectively as compared to the 5.3 ± 1.0% in control cells (Figure 3). Dracorhodin perchlorate-induced apoptosis in T24 cells were compatible with previously reported studies (He et al, 2011;Rasul et al, 2012a;Xia et al, 2005;Xia et al, 2006).…”

“…The results showed that procaspase-3 was activated in treated cells with 100 µM of dracorhodin perchlorate for 12, 24, and 48 h as compared to that of control cells (Figure 5). These findings are supported by previously studies (He et al, 2011;Rasul et al, 2012a;Xia et al, 2005;Xia et al, 2006). These results markedly showed that dracorhodin perchlorate induced caspase-dependent cell death in T24 cells.…”

“…Morphological changes were observed under phase contrast microscopy after treating cells with dracorhodin perchlorate resulting in the decreased number of cells as compared to control group and cells become rounded and shrinked, which were polygonal in untreated cells (data not shown). These results reveal that dracorhodin perchlorate can act as growth inhibitor of human bladder cancer T24 cells in a similar fashion as described in previous studies dealing with various other types of cancer cells including melanoma cells (Xia et al, 2005), leukemic cancer cells (Xia et al, 2006), prostate cancer cells (He et al, 2011) and gastric cancer cells (Rasul et al, 2012a).…”

“…An understanding of the molecular mechanism underlying dracorhodin perchlorate is just now emerging. In 2011, it was reported that dracorhodin perchlorate supperssed proliferation and induced apoptosis in human prostate cancer cells (He et al, 2011). Other studies have shown that dracorhodin perchlorate inhibited cell growth and triggered apoptosis in melanoma and leukemic cancer cells (Xia et al, 2005;Xia et al, 2006).…”