Esketamine induced apoptosis in human breast cancer cell line MDA-MB-468 and its mechanism
10.3760/cma.j.cn.115807-20221201-00346
- VernacularTitle:艾司氯胺酮诱导人乳腺癌细胞株MDA-MB-468凋亡及机制研究
- Author:
Qiuwen YIN
1
;
Qicai GUO
;
Xiumei MIAO
;
Aimei LI
;
Haiyan LIU
;
Dandan ZHAO
Author Information
1. 济宁医学院附属医院麻醉科,济宁 272000
- Keywords:
Esketamine;
Breast cancer;
Apoptosis;
Active oxygen;
PI3K/AKT signal path
- From:
Chinese Journal of Endocrine Surgery
2023;17(2):179-184
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore whether esketamine (ESK) can inhibit the proliferation and induce apoptosis of breast cancer cells, and explore the mechanism.Methods:CCK-8 assay was used to detect the inhibitory effect of ESK on the proliferation of breast cancer cells. Annexin V/PI staining was used to detect the morphological changes of cells; Apoptosis and reactive oxygen species were detected by flow cytometry. Western blot was used to detect apoptosis and pathway expression.Results:CCK-8 experiment results proved that ESK could inhibit the proliferation of breast cancer cells in a time-dependent manner. The survival rate of MDA-MB-468 cells treated with ESK at 20 μM was (35.47±2.61) %, which was statistically different from that treated with vinorelbine at the same concentration ( P<0.05). The IC50 value of ESK on MDA-MB-468 cells was (14.54±2.12) μM. After treatment with ESK, the mitochondrial membrane potential was significantly reduced. In the protein level, the expression of Cytochrome C, Bax and Caspase-3 was up-regulated, and the expression of Bcl-2 was down regulated, which induced the mitochondrial dependent apoptosis of MDA-MB-468 cells. ESK could up regulate the level of reactive oxygen species in MDA-MB-468 cells and regulate the expression of PI3K/AKT signaling pathway. Conclusions:ESK can inhibit the proliferation and migration of breast cancer cells and induce them to play a mitochondrial dependent apoptosis. Its mechanism is achieved by up regulating the level of ROS in breast cancer cells, thereby regulating the PI3K/AKT signaling pathway, which provides a theoretical basis for the development and utilization of Aln.