Pacilitaxel induces human nasopharyngeal carcinoma cell line CNE2 apoptosis and growth inhibition by suppressing PI3K/AKT/p53 signaling pathway.
- Author:
Tao LI
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Apoptosis Regulatory Proteins;
metabolism;
Carcinoma;
Cell Line, Tumor;
drug effects;
Flow Cytometry;
Humans;
Membrane Potentials;
Nasopharyngeal Carcinoma;
Nasopharyngeal Neoplasms;
metabolism;
pathology;
Paclitaxel;
pharmacology;
Phosphatidylinositol 3-Kinases;
metabolism;
Proto-Oncogene Proteins c-akt;
metabolism;
Signal Transduction;
Tumor Suppressor Protein p53;
metabolism
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2015;29(24):2147-2150
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect and mechanisms of the PTX on the human nasopharyngeal carcinoma cell line CNE2.
METHOD:Cells from CNE2 were cultured in vitro and the cells at logarithmic growth phase were processed with different concentration of PTX (0, 5, 10, 20) mol/L for 72h. MTT was used to evaluate the proliferation and flow cytometric analysis was utilized to detect membrane potential and apoptosis of CNE2 cells. The expression of PI3K, p-AKT, AKT, p53, p21, Caspase3, Cleavage-Caspase3, PARP, Cleavage-PARP, AIF, CytC, Bcl-2 and Bax in CNE2 cells were examined by Western Blot.
RESULT:The results showed that PTX could increase the apoptosis and the expression of Caspase3, PARP, CytC, AIF and Bax and reduce the proliferation, membrane potential and the expression of PI3K, p-AKT, p53, p21, Cleavage-PARP, Cleavage-Caspase3 and Bcl-2 in CNE2 cell in a concentration-dependent manner. However, PTX had no effect on the expression of AKT.
CONCLUSION:PTX can promote apoptosis and growth inhibition of human nasopharyngeal cancer cell line CNE2 and the mechanism involves suppressing PI3K/AKT/p53 signaling pathway.
