Effects of sodium selenite on the expressions of beta-catenin and its target cyclin D1 in colorectal cancer cells HCT 116 and SW480.
- Author:
Hui LUO
1
;
Yang YANG
;
Cai-Min XU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line, Tumor; Colorectal Neoplasms; metabolism; Cyclin D1; metabolism; HCT116 Cells; Humans; Sodium Selenite; pharmacology; beta Catenin; metabolism
- From: Acta Academiae Medicinae Sinicae 2011;33(6):654-658
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of sodium selenite on the expressions of beta-catenin and cyclin D1 in colorectal cancer cells HCT 116 and SW480.
METHODSHCT 116 and SW480 cells were treated by 10 micromol/L sodium selenite at different time points. The expressions and transcription of beta-catenin and cyclin D1 were detected by Western blot analysis and reverse transcriptase polymerase chain reaction (RT-PCR), respectively. Meanwhile, the impact of MG132 (a proteasome inhibitor) pretreatment on the expressions of beta-catenin and cyclin D1 was observed through Western blot analysis. The interaction between beta-catenin and T cell factor 4 (TCF4) after selenite treatment was evaluated using co-immunoprecipitation assay.
RESULTSSodium selenite inhibited the expression of beta-catenin and transcription of its target such as cyclin D1. MG132 pretreatment prevented the inhibition of beta-catenin signaling triggered by selenite in HCT 116 and SW480 cells. Furthermore, selenite treatment disrupted the interaction between beta-catenin and TCF4 in HCT 116 and SW480 cells.
CONCLUSIONSSodium selenite can lower the expression levels of beta-catenin and its target cyclin D1, during which the proteasome-mediated degradative pathway may be involved. The decreased interaction between beta-catenin and TCF4 due to sodium selenite may be also involved in the regulation of beta-catenin signaling.