Inhibitory effect of cyclopamine on metastatic ability of EC109 cells and its mechanism.
- Author:
Xiaoping ZUO
1
;
Zhiming QIN
;
Kaibin WANG
;
Xiangru ZHENG
;
Liqian CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line, Tumor; Esophageal Neoplasms; metabolism; pathology; Gene Expression Regulation, Neoplastic; Humans; Matrix Metalloproteinase 9; metabolism; Neoplasm Metastasis; RNA, Messenger; genetics; Signal Transduction; drug effects; Transcription Factors; metabolism; Vascular Endothelial Growth Factor A; metabolism; Veratrum Alkaloids; pharmacology; Zinc Finger Protein GLI1
- From: Journal of Southern Medical University 2012;32(12):1828-1832
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of cyclopamine on metastatic ability of human esophageal cancer EC109 cells and explore the possible mechanism.
METHODSTranswell chamber assay and angiogenesis assay were used to examine the metastatic ability, invasiveness and angiogenesis of EC109 cells treated with cyclopamine for 48 h. The expression of Gli-1 mRNA was detected using RT-PCR, and Western blotting was used to examine the protein expressions of Gli-1, matrix metalloproteinase-9 (MMP-9) and vascular endothelial growth factor (VEGF).
RESULTSInhibition of the hedgehog signaling pathway by cyclopamine suppressed the migration, invasion, and angiogenesis of EC109 cells. Cyclopamine treatment significantly lowered the expression of Gli-1 mRNA (P<0.05) and the protein expressions of Gli-1, MMP-9 and VEGF (P<0.05).
CONCLUSIONCyclopamine can significantly inhibit the metastatic capacity of EC109 cells possibly by down-regulating MMP-9 and VEGF expression as a result of Gli-1 inhibition.
