Journal
TUMOR BIOLOGY
Volume 36, Issue 11, Pages 8839-8844Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1007/s13277-015-3563-3
Keywords
Bladder cancer (BC); WNT signaling; MMP9; beta-Catenin
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Funding
- Shanghai Jiao Tong University Medical and Engineering Collaborative Research Fund Project [YG2012MS45]
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Bladder cancer (BC) is the most popular malignant urinary cancer, with the highest incidence and mortality of all genitourinary system tumors worldwide. To date, the molecular regulation of the metastasis of BC remains ill defined. Here, we examined the levels of matrix metallopeptidase 9 (MMP9) and nuclear beta-catenin in the BC specimen. We used lithium chloride (LiCl) to inhibit cytosol beta-catenin phosphorylation and degradation to increase nuclear beta-catenin levels in BC cells. We used IWP-2 to enhance cytosol beta-catenin phosphorylation and degradation to decrease nuclear beta-catenin levels in BC cells. We examined MMP9 levels in these experimental settings by quantitative reverse transcription-PCR (RT-qPCR), Western blot, and ELISA. The cell invasiveness was evaluated by Transwell cell assay. We found significantly higher levels of MMP9 and nuclear beta-catenin in human BC specimen with metastasis, compared to those without metastasis. Moreover, a strong correlation was detected between MMP9 and nuclear beta-catenin. LiCl significantly increased nuclear beta-catenin, resulting in MMP9 activation in BC cells. IWP-2 significantly decreased nuclear beta-catenin, resulting in MMP9 inhibition in BC cells. MMP9 regulated cell invasiveness. Together, these data suggest that the WNT signaling pathway regulates metastasis of BC through activation of MMP9. Therapies targeting the WNT signaling pathway may be a promising treatment for BC.
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