AZD9291 suppresses proliferation and migration of nasopharyngeal carcinoma cells by inhibiting the PI3K-AKT-mTOR pathway.
10.12122/j.issn.1673-4254.2022.09.18
- Author:
Heng Yi ZHANG
1
;
Jin Long PANG
2
;
Yu Han ZHANG
2
;
Yue MA
2
;
Fang Tian FAN
2
;
Hao LIU
2
Author Information
1. School of Clinical Medicine, Bengbu Medical College, Bengbu 233000, China.
2. School of Pharmacy, Bengbu Medical College//Anhui Biochemical Pharmaceutical Engineering Technology Research Center, Bengbu 233000, China.
- Publication Type:Journal Article
- Keywords:
AZD9291;
epidermal growth factor receptor tyrosine kinase inhibitor;
migration;
nasopharyngeal carcinoma;
proliferation
- MeSH:
Acrylamides;
Aniline Compounds;
Cell Line, Tumor;
Cell Movement;
Cell Proliferation;
ErbB Receptors;
Humans;
Indoles;
Nasopharyngeal Carcinoma/pathology*;
Nasopharyngeal Neoplasms/pathology*;
Phosphatidylinositol 3-Kinases/metabolism*;
Proto-Oncogene Proteins c-akt/metabolism*;
Pyrimidines;
TOR Serine-Threonine Kinases/metabolism*
- From:
Journal of Southern Medical University
2022;42(9):1403-1409
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effects of AZD9291 on the proliferation and migration of nasopharyngeal carcinoma cells.
METHODS:Nasopharyngeal carcinoma HNE1 and CNE2Z cells were treated with AZD9291 at the doses of 0.5, 1, 2, 4, and 8 μmol/L and at the doses of 1, 2, 4, 8, and 16 μmol/L, respectively. Cell survival was measured using CCK8 assay, and proliferation inhibition of the cells after AZD9291 treatment was examined with colony-forming assay; the cell repair and migration abilities were determined using scratch assay and Transwell experiment. The expressions of EGFR-related signaling proteins and migration-related proteins were detected using Western blotting.
RESULTS:The results of CCK8 assay and colonyforming assay showed that AZD9291 significantly inhibited the viability and proliferation of both HNE1 and CNE2Z cells (P < 0.01). AZD9291 treatment also attenuated the migration ability of HNE1 and CNE2Z cells (P < 0.01). Western blotting showed that, as the concentration of AZD9291 increased, the expression levels of the proteins involved in the PI3K-AKT-mTOR signaling pathway were lowered progressively (P < 0.01), resulting in inhibition of migration of HNE1 and CNE2Z cells (P < 0.01).
CONCLUSION:AZD9291 suppresses proliferation and attenuates repair and migration capacities of nasopharyngeal carcinoma cells by inhibiting the EGFR/PI3K/AKT/mTOR signaling pathway, suggesting the potential value of AZD9291 in the treatment of nasopharyngeal carcinoma.
