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Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling
Journal article   Open access   Peer reviewed

Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling

Ryan Kolb, Nicholas Borcherding, Qing Xie, Qi Liu, Christopher Stipp, Katherine N Gibson-Corley, Chen Zhao, Yuewan Luo, Myung-Chul Kim, Hank H Qi, …
Oncogene, Vol.39(14), pp.2877-2889
04/2020
DOI: 10.1038/s41388-020-1203-x
PMCID: PMC7127950
PMID: 32042113
url
https://doi.org/10.1038/s41388-020-1203-xView
Published (Version of record) Open Access

Abstract

Aiming to identify immune molecules with a novel function in cancer pathogenesis, we found the cluster of differentiation 177 (CD177), a known neutrophil antigen, to be positively correlated with relapse-free, metastasis-free, or overall survival in breast cancer. In addition, CD177 expression is correlated with good prognosis in several other solid cancers including prostate, cervical, and lung. Focusing on breast cancer, we found that CD177 is expressed in normal breast epithelial cells and is significantly reduced in invasive cancers. Loss of CD177 leads to hyperproliferative mammary epithelium and contributes to breast cancer pathogenesis. Mechanistically, we found that CD177-deficiency is associated with an increase in β-catenin signaling. Here we identified CD177 as a novel regulator of mammary epithelial proliferation and breast cancer pathogenesis likely via the modulation of Wnt/β-catenin signaling pathway, a key signaling pathway involved in multiple cancer types.
Animals beta Catenin - metabolism Breast Neoplasms - metabolism Cell Differentiation - physiology Cell Line Cell Line, Tumor Cell Proliferation - physiology Epithelial Cells - metabolism Female Gene Expression Regulation, Neoplastic - physiology GPI-Linked Proteins - metabolism HEK293 Cells Humans Isoantigens - metabolism MCF-7 Cells Mice Mice, Inbred BALB C Receptors, Cell Surface - metabolism Signal Transduction - physiology Wnt Signaling Pathway - physiology

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