Propofol induces ROS‑mediated intrinsic apoptosis and migration in triple‑negative breast cancer cells
- Hao Wang
- Lidong Zhao
- Jing Wu
- Jiang Hong
- Songpo Wang
Affiliations: Department of Traditional Chinese Medicine, The General Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200080, P.R. China, Department of Internal and Emergency Medicine, The General Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200080, P.R. China, School of Pharmacy, Shanghai Jiaotong University, Shanghai 200080, P.R. China
- Published online on: May 13, 2020 https://doi.org/10.3892/ol.2020.11608
Copyright: © Wang
et al. This is an open access article distributed under the
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Propofol is widely applied in general anesthesia owing to its short effect and rapid recovery. Apart from its anesthetic advantages, propofol has also been observed to inhibit the growth of several types of cancer cells. Breast cancer is the most diagnosed cancer in females worldwide and triple negative breast cancer (TNBC) constitutes 15‑20% of all breast cancer cases. TNBC is characterized by a high recurrence rate, which is associated with its high mortality rate. The present study aimed to evaluate apoptosis in MDA‑MB‑468 cells treated with propofol. The Cell Counting Kit‑8 assay was used to assess proliferation in cells treated with different concentrations of propofol. In addition, Annexin V‑FITC was used to detect apoptosis. Furthermore, the generation of reactive oxygen species (ROS) was examined. The relative expression of proteins in the intrinsic apoptosis pathway, such as Bak, Bax, Bcl‑2, Cytochrome c, apoptotic peptidase‑activating factor 1 (Apaf‑1), Caspase 3 and Caspase 9, were calculated relative to GAPDH with western blot analysis. A wound healing assay was performed to examine the effect of propofol on MDA‑MB‑468 cell migration. The present study revealed that propofol inhibited the proliferation and increased the level of ROS in MDA‑MB‑468 cells. The expression levels of Cytochrome c, Apaf‑1, Bax, Bak and cleaved Caspase 3/9 were upregulated compared with GAPDH. The level of Bcl‑2 protein was upregulated by propofol at a concentration of 5 µM and downregulated at concentrations of 10 and 20 µM. In the wound‑healing assay, propofol reduced the scratch distance and area. Taken together, the results of the present study suggested that propofol may induce ROS‑mediated intrinsic apoptosis and promote migration in TNBC cells.