[Transfection of Axin Gene Down-regulates Expressions of beta-catenin and TCF-4 and Inhibits the Proliferation and Invasive Ability of Lung Cancer Cells.].

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.