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Cancer cell-intrinsic function of CD177 in attenuating β-catenin signaling
Paige N Kluz1,2, Ryan Kolb3, Qing Xie1,4
1Department of Pathology, University of Iowa, College of Medicine, Iowa City, IA, 52242-1109, USA.
Oncogene
|February 12, 2020
Summary
Cluster of differentiation 177 (CD177) is a novel molecule linked to better survival in breast and other cancers. Its loss promotes cancer growth by increasing Wnt/β-catenin signaling.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Cluster of differentiation 177 (CD177) is a known neutrophil antigen.
- Its role in solid tumor pathogenesis is largely unexplored.
Purpose of the Study:
- To identify novel immune molecules involved in cancer pathogenesis.
- To investigate the function of CD177 in breast cancer and other solid tumors.
Main Methods:
- Correlation analysis of CD177 expression with patient survival data.
- Analysis of CD177 expression in normal versus cancerous breast tissues.
- Investigation of CD177's role in mammary epithelial proliferation.
- Assessment of CD177's impact on Wnt/β-catenin signaling.
Main Results:
- CD177 expression positively correlates with improved relapse-free, metastasis-free, and overall survival in breast cancer.
- CD177 expression is also linked to good prognosis in prostate, cervical, and lung cancers.
- CD177 is downregulated in invasive breast cancers, and its loss promotes mammary epithelial hyperproliferation.
- CD177 deficiency is associated with increased β-catenin signaling.
Conclusions:
- CD177 is a novel regulator of mammary epithelial proliferation and breast cancer pathogenesis.
- CD177 likely modulates Wnt/β-catenin signaling, a critical pathway in multiple cancer types.
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