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Sci Rep. 2015 Jul 23;5:12465. doi: 10.1038/srep12465.

Blockade of Wnt/β-catenin signaling suppresses breast cancer metastasis by inhibiting CSC-like phenotype.

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1] Laboratory of Tumor Suppressor, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-840, Republic of Korea [2] Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Republic of Korea.
Department of Oral Pathology, School of Dentistry, and Institute of Oral Bioscience, Chonbuk National University, Jeonju, Republic of Korea.
Department of New Technology Development, Korea Health Industry Development Institute (KHIDI), Cheongju-si 363-700, Republic of Korea.
Department of Companion and Laboratory Animal Science, Kongju National University, Chungnam 314-702, Republic of Korea.
The Faculty of Liberal Arts, Jungwon University, Chungbuk, 367-805, Republic of Korea.


The identification of cancer stem cells (CSCs) represents an important milestone in the understanding of chemodrug resistance and cancer recurrence. More specifically, some studies have suggested that potential metastasis-initiating cells (MICs) might be present within small CSC populations. The targeting and eradication of these cells represents a potential strategy for significantly improving clinical outcomes. A number of studies have suggested that dysregulation of Wnt/β-catenin signaling occurs in human breast cancer. Consistent with these findings, our previous data have shown that the relative level of Wnt/β-catenin signaling activity in breast cancer stem cells (BCSCs) is significantly higher than that in bulk cancer cells. These results suggest that BCSCs could be sensitive to therapeutic approaches targeting Wnt/β-catenin signaling pathway. In this context, abnormal Wnt/β-catenin signaling activity may be an important clinical feature of breast cancer and a predictor of poor survival. We therefore hypothesized that Wnt/β-catenin signaling might regulate self-renewal and CSC migration, thereby enabling metastasis and systemic tumor dissemination in breast cancer. Here, we investigated the effects of inhibiting Wnt/β-catenin signaling on cancer cell migratory potential by examining the expression of CSC-related genes, and we examined how this pathway links metastatic potential with tumor formation in vitro and in vivo.

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