Effect of hyperthermia combined with paclitaxel on proliferation, apoptosis and cycle of human tongue squamous cell carcinoma cell line CAL-27
10.3760/cma.j.cn113030-20211026-00434
- VernacularTitle:热疗联合紫杉醇对人舌鳞癌细胞系CAL-27增殖、凋亡和周期影响
- Author:
Xuexiao ZHOU
1
;
Pei SHEN
;
Fan SHI
;
Yun SHAO
;
Yuan CONG
;
Ting XU
;
Shengzhi WANG
Author Information
1. 青岛大学口腔医学院，青岛 266003
- Keywords:
Hyperthermia;
Paclitaxel;
Cell proliferation;
Cell apoptosis;
Cell cycle;
Human tongue squamous cell carcinoma cell line
- From:
Chinese Journal of Radiation Oncology
2022;31(2):192-195
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the effect of hyperthermia combined with paclitaxel on the proliferation, apoptosis and cycle of human tongue squamous cell carcinoma cell line CAL-27, and to explore the underlying mechanism.Methods:The working concentration of paclitaxel was determined by CCK-8 assay, and the cultured CAL-27 cells were divided into the control, paclitaxel, 42℃ hyperthermia and combined treatment groups. The ability of cell proliferation was detected by colony formation assay, and the cell cycle and apoptosis were determined by flow cytometry. The expression levels of AKT, p-AKT, Bcl-2 and Bax proteins in each group were measured by Western blot.Results:Compared with the control group, the proliferation was significantly inhibited and the apoptosis of CAL-27 cells was significantly promoted in the combined treatment, hyperthermia and paclitaxel groups (all P<0.05), and the anti-proliferation and apoptosis-promoting effect in the combined treatment group was significantly better than those in the hyperthermia and paclitaxel groups (all P<0.05). Western blot showed that hyperthermia combined with paclitaxel could significantly up-regulate the expression level of Bax protein and significantly down-regulate the expression levels of P-AKT and Bcl-2 in CAL-27 cells (all P<0.05). Conclusions:Hyperthermia combined with paclitaxel can play a synergistic role in inhibiting proliferation and promoting apoptosis of tongue squamous cell carcinoma CAL-27 cells. The mechanism may be related to the inhibition of AKT activation and the activation of Bax/Bcl-2 apoptosis signaling pathway.
