Effect of Biejiajian Pills on Wnt/β-catenin signal pathway and DKK-1 and FrpHe gene expressions in hepatocellular carcinoma cells / 南方医科大学学报
Journal of Southern Medical University
;
(12): 30-33, 2013.
Article
in Chinese
| WPRIM
| ID: wpr-352314
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of Biejiajian Pills on Wnt signal pathway and its inhibitory gene (DKK-1 and FrpHe) expressions and explore the mechanism underlying the action of Biejiajian Pills to suppress the invasiveness of hepatocellular carcinoma.</p><p><b>METHODS</b>Twenty-four Wistar rats were randomized equally into 3 groups for gavage of normal saline and Biejiajian Pills at 20- and 10-fold clinical doses for 3 days. Blood samples were then collected from the rats, and the serum was separated and added in HepG2 cell cultures. After 48 h of culture, the cells were collected to determine the cellular content of β-catenin protein using flow cytometry and detect DKK-1 and FrpHe mRNA expressions using qRT-PCR.</p><p><b>RESULTS</b>HepG2 cells cultured in the presence of sera from rats fed with Biejiajian Pills showed significantly lowered β-catenin protein expression and obvious down-regulation of DKK-1 mRNA expression, and the effect was correlated with the doses of the drug administered. The expression of FrpHe mRNA showed no significant differences between the 3 groups.</p><p><b>CONCLUSIONS</b>Biejiajian Pills can effectively inhibit the invasiveness and migration of hepatocellular carcinoma cells, which is closely related to decreased expressions of β-catenin and DKK-1 to cause block of the Wnt/β-catenin signal pathway.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Pharmacology
/
Drugs, Chinese Herbal
/
Proto-Oncogene Proteins
/
Rats, Wistar
/
Carcinoma, Hepatocellular
/
Intercellular Signaling Peptides and Proteins
/
Wnt Proteins
/
Beta Catenin
/
Hep G2 Cells
Type of study:
Controlled clinical trial
Limits:
Animals
/
Humans
/
Male
Language:
Chinese
Journal:
Journal of Southern Medical University
Year:
2013
Type:
Article
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