De-Miao Zhu1, Wan-Li Xue1, Wei Tao1, Jin-Cheng Li1. 1. Department of Breast Surgery, The First Affiliated Hospital of Liaoning Medical University Jinzhou 121001, China.
Abstract
OBJECTIVE: To explore the biological effects of ray cartilage extract (RCE) on human breast cancer cell line MCF-7 and its mechanism. METHODS: MCF-7 cells were treated with RCE of different concentrations for different durations, and then MCF-7 cell proliferation was evaluated with MTT test, cell cycle was detected with flow cytometer and the protein levels of cyclin D1 and p21 were determined with Western blot. RESULTS: MTT test indicated that MCF-7 cell proliferation was inhibited by RCE with an optimal inhibiting concentration of 10 μmol/L and an optimal action time of 48 h. Flow cytometer displayed that with the time prolongation of RCE action, the cells in S phase were significantly increased, but the cells in G2/M phase were significantly decreased; and MCF-7 apoptosis significantly increased as compared with blank control group (all P<0.05). Western blot found that with the time prolongation of RCE action, the level of cyclin D1 was significantly decreased, but the level of p21 was significantly increased as compared with blank control group (all P<0.05). CONCLUSION: RCE inhibits MCF-7 cell proliferation via arresting MCF-7 cell transformation from S phase to G2 phase. This may be associated with regulating the expressions of cyclin D1 and p21. RCE may be used as a drug for treatment of breast cancer in the future.
OBJECTIVE: To explore the biological effects of ray cartilage extract (RCE) on humanbreast cancer cell line MCF-7 and its mechanism. METHODS: MCF-7 cells were treated with RCE of different concentrations for different durations, and then MCF-7 cell proliferation was evaluated with MTT test, cell cycle was detected with flow cytometer and the protein levels of cyclin D1 and p21 were determined with Western blot. RESULTS:MTT test indicated that MCF-7 cell proliferation was inhibited by RCE with an optimal inhibiting concentration of 10 μmol/L and an optimal action time of 48 h. Flow cytometer displayed that with the time prolongation of RCE action, the cells in S phase were significantly increased, but the cells in G2/M phase were significantly decreased; and MCF-7 apoptosis significantly increased as compared with blank control group (all P<0.05). Western blot found that with the time prolongation of RCE action, the level of cyclin D1 was significantly decreased, but the level of p21 was significantly increased as compared with blank control group (all P<0.05). CONCLUSION: RCE inhibits MCF-7 cell proliferation via arresting MCF-7 cell transformation from S phase to G2 phase. This may be associated with regulating the expressions of cyclin D1 and p21. RCE may be used as a drug for treatment of breast cancer in the future.
Entities:
Keywords:
Breast cancer; MCF-7 cell line; cyclin; ray cartilage extract
Authors: Christopher J Ormandy; Elizabeth A Musgrove; Rina Hui; Roger J Daly; Robert L Sutherland Journal: Breast Cancer Res Treat Date: 2003-04 Impact factor: 4.872
Authors: Somaia Elsheikh; Andrew R Green; Mohammed A Aleskandarany; Matthew Grainge; Claire E Paish; Maryou B K Lambros; Jorge S Reis-Filho; Ian O Ellis Journal: Breast Cancer Res Treat Date: 2007-07-26 Impact factor: 4.872
Authors: Jaqueline F Campos; Priscilla P de Toledo Espindola; Heron F V Torquato; Wagner D Vital; Giselle Z Justo; Denise B Silva; Carlos A Carollo; Kely de Picoli Souza; Edgar J Paredes-Gamero; Edson L Dos Santos Journal: Front Pharmacol Date: 2017-08-14 Impact factor: 5.810