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

Paige N. Kluz, Ryan Kolb, Qing Xie, Nicholas Borcherding, Qi Liu, Yuewan Luo, Myung Chul Kim, Linna Wang, Yinan Zhang, Wei Li, Christopher Stipp, Katherine N. Gibson-Corley, Chen Zhao, Hank H. Qi, Andrew Bellizzi, Andy W. Tao, Sonia Sugg, Ronald J. Weigel, Daohong Zhou, Xian ShenWeizhou Zhang

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)2877-2889
Number of pages13
Issue number14
StatePublished - Apr 2 2020
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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