Back to Search Start Over

Effects of CKMT1 on radiosensitivity of nasopharyngeal carcinoma cells.

Authors :
Lan, Ruilong
Huang, Fei
Chen, Ruiqing
Wang, Zeng
Chen, Junying
Fu, Lengxi
Zhang, Lurong
Zhong, Guangxian
Hong, Jinsheng
Source :
International Journal of Radiation Biology. May2019, Vol. 95 Issue 5, p597-606. 10p.
Publication Year :
2019

Abstract

Purpose: Radioresistance is an important factor for unsatisfactory prognosis in Nasopharyngeal carcinoma (NPC) patients. Ubiquitous mitochondrial creatine kinase (CKMT1) is always associated with malignancy in a variety of cancers. However, its significance in NPC progression and radiosensitivity remains unclear. The present study focused on investigating the effects of CKMT1 on NPC cell radiosensitivity. Material and methods: CKMT1 was overexpressed in NPC cell line CNE-1 or knocked out in CNE-2. Biological changes were detected after cells exposing to different doses of X-ray to determine the role of CKMT1 on NPC cell radiosensitivity. Results: CKMT1 promotes proliferation and migration in NPC cell lines CNE-1 and CNE-2. Overexpression of CKMT1 in CNE-1 cells enhanced colony formation rates, reduced G2/M phase cell cycle arrest, lowered apoptosis rate and c-PARP level, and elevated STAT3 phosphorylation level after radiation treatment. While knocking out CKMT1 using the CRISPR/Cas9 system in CNE-2 cells lowered colony formation rates, increased G2/M phase cell cycle arrest, apoptosis rates, and c-PARP levels, and decreased STAT3 phosphorylation in response to radiation treatment. Conclusions: NPC cells with higher CKMT1 exhibited lower radiosensitivity through promoting phosphorylation of STAT3. Our findings suggest that CKMT1 may be an alternative radiotherapeutic target in NPC therapy. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
09553002
Volume :
95
Issue :
5
Database :
Academic Search Index
Journal :
International Journal of Radiation Biology
Publication Type :
Academic Journal
Accession number :
136150136
Full Text :
https://doi.org/10.1080/09553002.2019.1554919