Dracorhodin perchlorate suppresses proliferation and induces apoptosis in human prostate cancer cell line PC-3
- J Huazhong Univ Sci Technolog Med Sci. 2011 Apr;31(2):215. doi: 10.1007/s11596-011-0255-0.
- 1. Department of Laboratory Animal Science, Nanchang University, Nanchang, 330006, China.
- 2. Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. [email protected].
- 3. Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
- 4. Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
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.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Apoptosis; Akt; PI3K; NF-κB; MDM-2/p53; Caspase; Reactive Oxygen Species (ROS); Toll-like Receptor (TLR); PARP
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Research Areas: Cancer