NDLI: MUC1 induces M2 type macrophage influx during postpartum mammary gland involution and triggers breast cancer

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MUC1 induces M2 type macrophage influx during postpartum mammary gland involution and triggers breast cancer

Content Provider	Semantic Scholar
Author	Li, Yuan Pang, Zhi Qiang Dong, Xinran Liao, Xiaodong Deng, Huayun Liao, Chunhua Liao, Yahui Chen, Guoqiang Huang, Lei
Copyright Year	2018
Abstract	The microenvironment of postpartum mammary gland involution (PMI) has been linked to the increased risk of breast cancer and poor outcome of patients. Nevertheless the mechanism underlying regulates the microenvironment remains largely unknown. MUC1, which is abnormally overexpressed in most breast cancer, is physiologically expressed in PMI. Using MUC1 cytoplasm domain (MUC1-CD) transgenic mice, we reveal that the overexpression of MUC1-CD in mammary epithelial cells increases M2 type macrophage infiltration in PMI. By sustain activating p50, MUC1 upregulates M2 macrophage chemo-attractants and the anti-apoptotic protein Bcl-xL. Because of the tumor promotional microenvironments and reduced apoptosis, MUC1-CD delays PMI process and results in atypical phenotype in multiparous mice mammary. This finding is further supported by the positive association between the expression of MUC1 and p50 in Luminal A and Luminal B subtypes through analyzing breast cancer databases. Taken together, our study demonstrates that MUC1-CD plays an important role in regulating microenvironment of PMI and promoting postpartum mammary tumorigenicity, providing novel prevention and treatment strategies against postpartum breast cancer.
Starting Page	3446
Ending Page	3458
Page Count	13
File Format	PDF HTM / HTML
DOI	10.18632/oncotarget.23316
PubMed reference number	29423058
Journal	Medline
Volume Number	9
Alternate Webpage(s)	http://www.oncotarget.com/index.php?journal=oncotarget&op=download&page=article&path%5B%5D=23316&path%5B%5D=73486
Alternate Webpage(s)	https://doi.org/10.18632/oncotarget.23316
Journal	Oncotarget
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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