Journal
STEM CELLS
Volume 33, Issue 10, Pages 2913-2924Publisher
WILEY-BLACKWELL
DOI: 10.1002/stem.2083
Keywords
Breast cancer; LGR5; EMT; Wnt/beta-Catenin; Cancer stem cell
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Funding
- National Natural Science Foundation of China [81472575, 81272514, 81472469, 81302318, 81301798, 31030061]
- China Postdoctoral Science Foundation [2012M520075, 2014T70834, 2014M550447]
- Science and Technology Planning Project of Guangzhou and Guangdong [2014J4100169, 2013B060300009]
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The cancer stem cell (CSC) hypothesis suggests that a subset of cancer cells possesses stem cell properties and is crucial in tumor initiation, metastasis, and drug resistance. To determine the mechanism of CSCs in breast cancer, we focused on LGR5, a marker of adult stem cells that potentially serves as a functional factor in CSCs. LGR5 overexpression was detected in breast cancer and significantly associated with breast cancer recurrence and poor outcome. LGR5 promoted cell mobility, tumor formation, and epithelial-mesenchymal transition in breast cancer cells by activating Wnt/beta-catenin signaling. In addition, LGR5 was more highly expressed in tumorspheres and increased the stemness of breast cancer cells. Compared with LGR5 lowexpression (LGR5(low)) cells, LGR5(high) cells exhibited CSC/tumor-initiating cell-like properties, including the formation of self-renewing spheres and high tumorigenicity. Importantly, our studies indicate that LGR5 activation of Wnt/beta-catenin signaling is a possible mechanism to regulate breast CSC/tumor-initiating cell renewal. These findings indicate that LGR5 not only participates in carcinogenesis but also maintained stemness by activating Wnt/beta-catenin signaling in breast cancer.
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