Role of chloride channels in gambogic acid-induced apoptosis of poorly differentiated nasopharyngeal carcinoma cells.
- Author:
Zhi-quan BAI
1
;
Hua-rong LI
;
Hai-feng ZHANG
;
Shan-wen LIU
;
Lin-yan ZHU
;
Wen-cai YE
;
Li-xin CHEN
;
Li-wei WANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Line, Tumor; Chloride Channels; drug effects; physiology; Humans; Nasopharyngeal Neoplasms; pathology; Patch-Clamp Techniques; Xanthones; pharmacology
- From: Journal of Southern Medical University 2011;31(8):1304-1308
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of chloride channels in the apoptosis of poorly differentiated nasopharyngeal carcinoma CNE-2Z cells induced by gambogic acid (GA).
METHODSMTT assay was applied to detect the proliferation of CNE-2Z cells after GA treatment, and the cell apoptosis was detected by Hoechst 33342 staining. Whole-cell patch clamp technique was employed to record GA-activated Cl(-) currents in the cells.
RESULTSGA inhibited the cell proliferation in a time- and concentration-dependent manner with an IC(50) of 3.1 µmol/L for a 48-h treatment. The apoptosis-inducing effect of 8 µmol/L GA was attenuated by the chloride channel blocker NPPB (100 µmol/L) and tamoxifen (20 µmol/L). GA induced an outward-rectified Cl(-) current in the cells, which was significantly inhibited by NPPB.
CONCLUSIONGA suppresses cell proliferation and induces apoptosis by activating Cl(-) channels in CNE-2Z cells, suggesting the important role of Cl(-) channels in GA-induced apoptosis.
