Effect and mechanisms of TET on human gastric carcinoma cell line SGC7901 and SGC7901/ADR.
- Author:
Yong LI
1
;
Qun ZHAO
2
;
Bi-Bo TAN
2
;
Li-Qiao FAN
2
;
Qing-Wei LIU
2
;
Zhi-Kai JIAO
2
;
Xue-Feng ZHAO
2
;
Ying-Jie HAO
2
Author Information
- Publication Type:Journal Article
- MeSH: ATP Binding Cassette Transporter, Sub-Family B; metabolism; Benzylisoquinolines; pharmacology; Cell Line, Tumor; Drug Resistance, Multiple; drug effects; genetics; Drug Resistance, Neoplasm; drug effects; genetics; Humans; Kruppel-Like Transcription Factors; metabolism; Multidrug Resistance-Associated Proteins; metabolism; Stomach Neoplasms; metabolism; Zinc Fingers; genetics
- From: Chinese Journal of Integrated Traditional and Western Medicine 2014;34(1):66-70
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of tetrandrine (TET) on zinc finger protein 139 (ZNF139) and multidrug resistance (MDR) of human gastric carcinoma cell lines and possible mechanisms.
METHODSCultured SGC7901 and SGC7901/ADR were treated with TET (0.5, 1.0, 1.5, 2.0, and 2.5 microg/mL), then inhibition rates were measured by MTT assay in vitro. The expressions of ZNF139, MRP-1, MDR1, and GST-pi were detected by RT-PCR. The correlation between ZNF139 and each multidrug resistance factor was analyzed using Spearman correlation analysis, and the coefficient correlation was calculated.
RESULTSThe inhibition rate of TET (< or = 2.0 microg/mL) for SGC7901 and SGC7901/ADR was less than 10% with MTT assay. Expressions of ZNF139, MRP-1, MDR1, and GST-pi mRNA were higher in SGC7901/ADR than in SGC7901 (all P < 0.05). The expressions of ZNF139, MRP-1, MDR1, and GST--pi were down-regulated in SGC7901/ADR cells efficiently (all P < 0.01). Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05).
CONCLUSIONTET could achieve MDR reversion in gastric cancer cells by down-regulating the expression of ZNF139, MRP-1, and MDR1.