Deltonin induces apoptosis in MDA‑MB‑231 human breast cancer cells via reactive oxygen species‑mediated mitochondrial dysfunction and ERK/AKT signaling pathways.
机构：[1]Laboratory of Ethnopharmacology, Regenerative Medicine Research Center, Institute for Nanobiomedical Technology and Membrane Biology, West China Hospital/Medical School, Sichuan University, Sichuan 610041四川大学华西医院[2]State Key Laboratory of Oral Disease, West China Hospital of Stomatology,Sichuan University, Chengdu 610041, P.R. China
Deltonin, a steroidal saponin isolated from Dioscorea zingiberensis Wright, exhibits high cytotoxic activity in cancer cells. In the present study, the effects of deltonin on cell proliferation and apoptosis were evaluated in the MDA‑MB‑231 human breast carcinoma cell line. Following treatment with deltonin, the viability of MDA‑MB‑231 cells was analyzed using MTT assay and apoptosis, mitochondrial membrane potential (∆Ψm) alternation and intracellular reactive oxygen species (ROS) generation was determined by flow cytometry. In addition, western blot analysis was performed to examine the expression of apoptosis‑associated proteins. The results demonstrated that deltonin induced apoptosis in MDA‑MB‑231 cells in a time‑ and concentration‑dependent manner. Apoptosis was associated with depolarization of ∆Ψm and time‑dependent ROS generation. Deltonin treatment also resulted in Bax upregulation, Bcl-2 downregulation, activation of caspase‑3 and ‑8 and poly (ADP ribose) polymerase cleavage. Decreased levels of phosphorylated extracellular signal‑regulated kinase (ERK) and phosphorylated AKT were also observed. Results indicate that the proliferation inhibitory effect of deltonin is associated with its apoptosis‑inducing effect, which may correlate with ROS‑mediated mitochondrial dysfunction as well as activation of the ERK/AKT signaling pathways. Therefore, deltonin may be a potential chemotherapeutic agent for the treatment of breast cancer.
基金：
National Major Scientific and Technological Special Project (no. 2009ZX09102-045), National 12th 5-Year Plan Project of China (no. 2011BAJ07B04) and the National Natural Science Foundation of China (no. 20972105).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2013]版：
大类|4 区医学
小类|4 区医学：研究与实验4 区肿瘤学
最新[2023]版：
大类|3 区医学
小类|4 区医学：研究与实验4 区肿瘤学
第一作者：
第一作者机构：[1]Laboratory of Ethnopharmacology, Regenerative Medicine Research Center, Institute for Nanobiomedical Technology and Membrane Biology, West China Hospital/Medical School, Sichuan University, Sichuan 610041
共同第一作者：
通讯作者：
通讯机构：[1]Laboratory of Ethnopharmacology, Regenerative Medicine Research Center, Institute for Nanobiomedical Technology and Membrane Biology, West China Hospital/Medical School, Sichuan University, Sichuan 610041[2]State Key Laboratory of Oral Disease, West China Hospital of Stomatology,Sichuan University, Chengdu 610041, P.R. China[*1]Laboratory of Ethnopharmacology, Regenerative Medicine Research Center, Institute for Nanobiomedical Technology and Membrane Biology, West China Hospital/Medical School, Sichuan University, 1 Keyuan 4 Road, No. 1 Gaopeng Avenue, Sichuan 610041, P.R. China[*2]State Key Laboratory of Oral Disease, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, P.R. China
推荐引用方式(GB/T 7714)：
Zhang Shiyuan,He Yang,Tong Qingyi,et al.Deltonin induces apoptosis in MDA‑MB‑231 human breast cancer cells via reactive oxygen species‑mediated mitochondrial dysfunction and ERK/AKT signaling pathways.[J].Molecular medicine reports.2013,7(3):1038-44.doi:10.3892/mmr.2013.1273.
APA：
Zhang Shiyuan,He Yang,Tong Qingyi,Chen Qianming,Wu Xiaohua&Huang Wen.(2013).Deltonin induces apoptosis in MDA‑MB‑231 human breast cancer cells via reactive oxygen species‑mediated mitochondrial dysfunction and ERK/AKT signaling pathways..Molecular medicine reports,7,(3)
MLA：
Zhang Shiyuan,et al."Deltonin induces apoptosis in MDA‑MB‑231 human breast cancer cells via reactive oxygen species‑mediated mitochondrial dysfunction and ERK/AKT signaling pathways.".Molecular medicine reports 7..3(2013):1038-44
