Abstract | BACKGROUND: Axin is an important negative regulator of Wnt signaling pathway. It can induce the phosphorylation and degradation of beta-catenin. The reduced expression of axin or high expression of beta-catenin and TCF-4 were associated with malignant proliferation in many tumors. The aim of this study is to examine the relationships among the expressions and locations of axin, beta-catenin and other relevant molecules, and the roles of axin on proliferation, invasive ability and apoptosis of lung cancer cells. METHODS: The axin cDNA was transfected into lung cancer BE1 cell line which has very low axin expression. The levels of expression and location of axin, beta-catenin and TCF-4 before and after transfection were detected using immunofluorescence. The mRNA levels of expression of axin, beta-catenin and TCF-4 were examined using reverse transcription-polymerase chain reaction (RT-PCR). The apoptosis, proliferation and invasive ability of lung cancer cells before and after transfection were examined with flow cytometry, MTT and transwell methods. RESULTS: After transfection of axin gene into BE1 cells (BE1-axin cells), axin mRNA and protein were overexpressed significantly. Meanwhile, the protein expression of beta-catenin and mRNA expression of TCF-4 were decreased significantly in BE1-axin cells than that in BE1 or vector control cells. The flow cytometry revealed that the apoptosis rate of BE1-axin cells was enhanced, but MTT and Transwell assay indicated that the proliferation and invasive ability were decreased significantly in BE1-axin cells than those in BE1 or vector control cells. CONCLUSIONS: The overexpression of axin could down-regulate the protein expression of beta-catenin and the transcription of TCF-4, and inhibit the proliferation and invasive ability of lung cancer cells.
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Authors | Shuli Liu, Hongtao Xu, Lianhe Yang, Qingchang Li, Qiang Wei, Enhua Wang |
Journal | Zhongguo fei ai za zhi = Chinese journal of lung cancer
(Zhongguo Fei Ai Za Zhi)
Vol. 12
Issue 4
Pg. 277-82
(Apr 20 2009)
ISSN: 1999-6187 [Electronic] China |
PMID | 20719112
(Publication Type: English Abstract, Journal Article)
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