Yaoyuan Li1, Jieqing Hu, Hui Huang, Yonghe He. 1. Department of Oncology, Guang'an men Hospital Affiliated to China Academy of Chinese Medical Sciences, Beijing 100053, China.
Abstract
OBJECTIVE: To study the possible roles of Jinlong capsule (JLC) on the proliferation and apoptosis of human pancreatic cancer cells BxPC-3. METHODS: The human pancreatic cancer cells BxPC-3 were treated with JLC at the concentration of 0.05-1.00 mg/mL for 24-120 h. The inhibition rate of JLC on human pancreatic cancer cells BxPC-3 was detected by 3-(4,5-dimethiylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry was employed to measure cell apoptosis using Annexin V-FITC/Propidium iodide (AV-FITC/PI) method. Cell cycles were determined by PI staining. The expression of 5100 Calcium binding protein A4 (S100A4) in cell matrix was measured by enzyme-linked immunosorbent assay (ELISA). The expression levels of apoptosis-related protein such as BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3), B-cell lymphoma/leukemia-2 (Bcl-2) and Cys-teinylaspartate specific proteinase 3 (Caspase-3) were detected by Western blotting. RESULTS: JLC significantly inhibited the proliferation of human pancreatic cancer cells BxPC-3 in a dose-dependent and time-dependent manner. JLC promoted cell apoptosis and maintained cell cycle in S and G2/M phase rather than G1/G0 phase. The expression of 5100A4 in the cell matrix was reduced. The expression of cell apoptotic protein BNIP3 was increased while Bcl-2 was decreased. CONCLUSION: JLC can inhibit the proliferation of human pancreatic cancer cells BxPC-3 by stimulating cell apoptosis, arresting the cell cycle at S and G2/M phase which blocks the circulation of normal cell cycle and reducing the expression of S100A4 protein. Higher pro-apoptosis protein BNIP3 and lower anti-apoptosis protein Bcl-2 levels were found, which may be related to the apoptotic effects of JLC.
OBJECTIVE: To study the possible roles of Jinlong capsule (JLC) on the proliferation and apoptosis of humanpancreatic cancer cells BxPC-3. METHODS: The humanpancreatic cancer cells BxPC-3 were treated with JLC at the concentration of 0.05-1.00 mg/mL for 24-120 h. The inhibition rate of JLC on humanpancreatic cancer cells BxPC-3 was detected by 3-(4,5-dimethiylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry was employed to measure cell apoptosis using Annexin V-FITC/Propidium iodide (AV-FITC/PI) method. Cell cycles were determined by PI staining. The expression of 5100 Calcium binding protein A4 (S100A4) in cell matrix was measured by enzyme-linked immunosorbent assay (ELISA). The expression levels of apoptosis-related protein such as BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3), B-cell lymphoma/leukemia-2 (Bcl-2) and Cys-teinylaspartate specific proteinase 3 (Caspase-3) were detected by Western blotting. RESULTS: JLC significantly inhibited the proliferation of humanpancreatic cancer cells BxPC-3 in a dose-dependent and time-dependent manner. JLC promoted cell apoptosis and maintained cell cycle in S and G2/M phase rather than G1/G0 phase. The expression of 5100A4 in the cell matrix was reduced. The expression of cell apoptotic protein BNIP3 was increased while Bcl-2 was decreased. CONCLUSION: JLC can inhibit the proliferation of humanpancreatic cancer cells BxPC-3 by stimulating cell apoptosis, arresting the cell cycle at S and G2/M phase which blocks the circulation of normal cell cycle and reducing the expression of S100A4 protein. Higher pro-apoptosis protein BNIP3 and lower anti-apoptosis protein Bcl-2 levels were found, which may be related to the apoptotic effects of JLC.