Effect of ubiquitous mitochondrial creatine kinase on cisplatin sensitivity of human nasopharyngeal carcinoma cell line CNE-1
10.3760/cma.j.issn.1673-0860.2018.07.008
- VernacularTitle: 线粒体肌酸激酶1对人鼻咽癌细胞株CNE－1顺铂敏感性的作用研究
- Author:
Ruilong LAN
1
;
Fei HUANG
1
;
Ruiqing CHEN
1
;
Zeng WANG
1
;
Junying CHEN
1
;
Jing′an LIN
1
;
Lengxi FU
1
Author Information
1. Central Lab, First Affiliated Hospital of Fujian Medical University, Fuzhou, China 350005
- Publication Type:Journal Article
- Keywords:
Nasopharyngeal neoplasms;
Ubiquitous mitochondrial creatine kinase;
Cisplatin
- From:
Chinese Journal of Otorhinolaryngology Head and Neck Surgery
2018;53(7):524-529
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of ubiquitous mitochondrial creatine kinase 1(CKMT1) on the sensitivity of human nasopharyngeal carcinoma cell line CNE-1 to DDP.
Methods:CNE-1 cells were transiently transfected with CKMT1 overexpression (CKMT1) or empty vector (EV). The growth curve and DDP IC50 were developed by MTT assay, plate clone formation assay was performed by gradient concentration of DDP treatment, cell cycle and apoptosis were detected by flow cytometry, levels of apoptosis related protein Bax/Bcl-2/C-PARP and the transcription factor p-STAT3-Tyr705 were detected by Western Blot.
Results:The transfection efficiencies of CKMT1 and EV were more than 90% with a higher proliferation rate in the CKMT1-transfected cells. However, the CKMT1-transfected cells had a DDP IC50 of 2.76 μmol/L, which was significantly lower than that of 4.60 μmol/L in the EV-transfected cells (P<0.01). With the treatment of certain concentration of DDP, the CKMT1-transfected cells had a lower clone formation rate, the cell cycle arrested more obviously in G2/M phase, and the apoptosis rate was higher (P<0.01), with higher levels of Bax/C-PARP (P<0.05 or P<0.01), but lower levels of Bcl-2 (P<0.01) and p-STAT3-Tyr705 (P<0.01), compare with the EV-transfected cells.
Conclusions:CKMT1 may inhibit the activation of STAT3, increasing the sensitivity of CNE-1 to chemotherapeutic drug DDP.
