Effects end mechanisms of curcumol beta-cyclodextrin compound on the proliferation and apoptosls of esophageal carcinoma cell line TE-1.
- Author:
Zhao JING
1
;
Cong-Ying XIE
;
Zhi-Qin WU
;
Fang XU
;
Chang-Lin ZOU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Esophageal Neoplasms; pathology; Humans; Sesquiterpenes; pharmacology; beta-Cyclodextrins; pharmacology
- From: Chinese Journal of Integrated Traditional and Western Medicine 2013;33(1):85-89
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects and mechanisms of Curcumol beta-cyclodextrin Compound (CbetaC) on the proliferation and apoptosis of esophageal carcinoma cell line TE-1.
METHODSThe CbetaC was prepared by saturated solution and confirmed by infrared absorption spectroscopy. The effects of CbetaC (at 25, 50, 100 mg/L) on the proliferation of human esophageal carcinoma cell line TE-1 in vitro was analyzed by MTT assay. The cell cycles and apoptosis were detected by flow cytometer. The relative expression of survivin mRNA was detected by real-time fluorescent quantitative PCR and calculated by the 2(-deltaCt) method. The protein expression of survivin was measured by Western blot.
RESULTSCompared with the control group, results of MTT showed that CbetaC at each dose significantly inhibited the proliferation of TE-1 cells in a dose-dependent manner (P < 0.05). The results of flow cytometry showed that CbetaC resulted in the cell cycle arrest at G0/G1 and G2/M phase, and promoted the cell apoptosis. Besides, when compared with the control group, the protein and mRNA expressions of survivin obviously decreased in each CbetaC group (P < 0.05).
CONCLUSIONSCbetaC could inhibit the proliferation of esophageal carcinoma cell TE-1 and promote the apoptosis. Its inhibition on the survivin expression was correlated with its inhibition on the malignant phenotypes of esophageal carcinoma cells.
