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 Shen; Weizhou Zhang

doi:10.1038/s41388-020-1203-x

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

Division of Laboratory and Genomic Medicine

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

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.

Original language	English
Pages (from-to)	2877-2889
Number of pages	13
Journal	Oncogene
Volume	39
Issue number	14
DOIs	https://doi.org/10.1038/s41388-020-1203-x
State	Published - Apr 2 2020

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Kluz, P. N., Kolb, R., Xie, Q., Borcherding, N., Liu, Q., Luo, Y., Kim, M. C., Wang, L., Zhang, Y., Li, W., Stipp, C., Gibson-Corley, K. N., Zhao, C., Qi, H. H., Bellizzi, A., Tao, A. W., Sugg, S., Weigel, R. J., Zhou, D., ... Zhang, W. (2020). Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling. Oncogene, 39(14), 2877-2889. https://doi.org/10.1038/s41388-020-1203-x

@article{041be55893884d59bb35f837b08dd242,

title = "Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling",

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.",

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

note = "Publisher Copyright: {\textcopyright} 2020, The Author(s), under exclusive licence to Springer Nature Limited.",

year = "2020",

month = apr,

day = "2",

doi = "10.1038/s41388-020-1203-x",

language = "English",

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Kluz, PN, Kolb, R, Xie, Q, Borcherding, N, Liu, Q, Luo, Y, Kim, MC, Wang, L, Zhang, Y, Li, W, Stipp, C, Gibson-Corley, KN, Zhao, C, Qi, HH, Bellizzi, A, Tao, AW, Sugg, S, Weigel, RJ, Zhou, D, Shen, X & Zhang, W 2020, 'Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling', Oncogene, vol. 39, no. 14, pp. 2877-2889. https://doi.org/10.1038/s41388-020-1203-x

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T1 - Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling

AU - Kluz, Paige N.

AU - Kolb, Ryan

AU - Xie, Qing

AU - Borcherding, Nicholas

AU - Liu, Qi

AU - Luo, Yuewan

AU - Kim, Myung Chul

AU - Wang, Linna

AU - Zhang, Yinan

AU - Li, Wei

AU - Stipp, Christopher

AU - Gibson-Corley, Katherine N.

AU - Zhao, Chen

AU - Qi, Hank H.

AU - Bellizzi, Andrew

AU - Tao, Andy W.

AU - Sugg, Sonia

AU - Weigel, Ronald J.

AU - Zhou, Daohong

AU - Shen, Xian

AU - Zhang, Weizhou

PY - 2020/4/2

Y1 - 2020/4/2

N2 - 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.

AB - 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.

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JO - Oncogene

JF - Oncogene

IS - 14

ER -

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

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