Keqiang Zhang1, Yuwei Li2. 1. a The Medical Department in Second Hospital of Jilin University , Changchun , PR China ; 2. b Nursing College of Jilin University , Changchun , PR China.
Abstract
CONTEXT: Breast cancer seriously harms the health of women and there are currently few therapeutic options for patients with breast cancer. OBJECTIVE: Effects of ginsenoside compound K (CK) in combination with cisplatin (DDP) on the proliferation, apoptosis, and epithelial mesenchymal transition (EMT) of MCF-7 cells were studied. MATERIALS AND METHODS: MCF-7 cells were divided into CK (50 μmol/L) group, DDP (10 mg/L) group, CK (50 μmol/L) +DDP (10 mg/L) group, and control (CON) group. The cells in the CON group were not treated with any drugs. Proliferation, apoptosis, expression of E-cadherin, N-cadherin, vimentin, protein kinase B (Akt), phosphorylated Akt (p-Akt), and level of fibronectin (FN) in MCF-7 cells were detected by methyl thiazolyl tetrazolium (MTT), flow cytometry, western blotting, and enzyme-linked immuno sorbent assay (ELISA), respectively. RESULTS: The proliferation inhibition rates in CK, DDP, and CK + DDP groups at 48 h were 19.18 ± 2.25, 21.34 ± 2.84, and 43.37 ± 5.62, respectively. The apoptosis rates were 2.85 ± 0.56, 13.37 ± 2.28, 20.04 ± 2.92, and 30.78 ± 4.64 at 24 h and 3.14 ± 0.72, 20.36 ± 3.28, 27.58 ± 4.09, and 41.62 ± 5.83 at 48 h in CON, CK, DDP, and CK + DDP groups, respectively. CK or DDP alone and their combination all could reduce the levels of N-cadherin, vimentin, p-Akt/Akt, and FN and elevate level of E-cadherin. DISCUSSION AND CONCLUSION: Both CK and DDP can inhibit the proliferation, EMT, and induce the apoptosis in MCF-7 cells, which may be related to the PI3K/Akt pathway. In addition, the combination of CK with DDP can produce a better effect.
CONTEXT: Breast cancer seriously harms the health of women and there are currently few therapeutic options for patients with breast cancer. OBJECTIVE: Effects of ginsenoside compound K (CK) in combination with cisplatin (DDP) on the proliferation, apoptosis, and epithelial mesenchymal transition (EMT) of MCF-7 cells were studied. MATERIALS AND METHODS: MCF-7 cells were divided into CK (50 μmol/L) group, DDP (10 mg/L) group, CK (50 μmol/L) +DDP (10 mg/L) group, and control (CON) group. The cells in the CON group were not treated with any drugs. Proliferation, apoptosis, expression of E-cadherin, N-cadherin, vimentin, protein kinase B (Akt), phosphorylated Akt (p-Akt), and level of fibronectin (FN) in MCF-7 cells were detected by methyl thiazolyl tetrazolium (MTT), flow cytometry, western blotting, and enzyme-linked immuno sorbent assay (ELISA), respectively. RESULTS: The proliferation inhibition rates in CK, DDP, and CK + DDP groups at 48 h were 19.18 ± 2.25, 21.34 ± 2.84, and 43.37 ± 5.62, respectively. The apoptosis rates were 2.85 ± 0.56, 13.37 ± 2.28, 20.04 ± 2.92, and 30.78 ± 4.64 at 24 h and 3.14 ± 0.72, 20.36 ± 3.28, 27.58 ± 4.09, and 41.62 ± 5.83 at 48 h in CON, CK, DDP, and CK + DDP groups, respectively. CK or DDP alone and their combination all could reduce the levels of N-cadherin, vimentin, p-Akt/Akt, and FN and elevate level of E-cadherin. DISCUSSION AND CONCLUSION: Both CK and DDP can inhibit the proliferation, EMT, and induce the apoptosis in MCF-7 cells, which may be related to the PI3K/Akt pathway. In addition, the combination of CK with DDP can produce a better effect.