BPIFB1 promotes metastasis of hormone receptor‐positive breast cancer via inducing macrophage M2 ‐like polarization

Metastasis is an important factor affecting the prognosis of hormone receptor‐positive breast cancer (BC). However, the molecular basis for migration and invasion of tumor cells remains poorly understood. Here, we identify that bactericidal/permeability‐increasing‐fold‐containing family B member 1 (...

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Published inCancer science Vol. 114; no. 11; pp. 4157 - 4171
Main Authors Hu, Anbang, Liu, Yansong, Zhang, Hanyu, Wang, Ting, Zhang, Jiarui, Cheng, Weilun, Yu, Tianshui, Duan, Yunqiang, Feng, Jianyuan, Chen, Ziang, Ding, Yu, Li, Yanling, Li, Mingcui, Rong, Zhiyuan, Shang, Yuhang, Shakila, Suborna S., Zou, Yiyun, Ma, Fei, Guo, Baoliang
Format Journal Article
LanguageEnglish
Published Tokyo John Wiley & Sons, Inc 01.11.2023
John Wiley and Sons Inc
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ISSN1347-9032
1349-7006
1349-7006
DOI10.1111/cas.15957

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Summary:Metastasis is an important factor affecting the prognosis of hormone receptor‐positive breast cancer (BC). However, the molecular basis for migration and invasion of tumor cells remains poorly understood. Here, we identify that bactericidal/permeability‐increasing‐fold‐containing family B member 1 (BPIFB1), which plays an important role in innate immunity, is significantly elevated in breast cancer and associated with lymph node metastasis. High expression of BPIFB1 and its coding mRNA are significantly associated with poor prognosis of hormone receptor‐positive BC. Using enrichment analysis and constructing immune infiltration evaluation, we predict the potential ability of BPIFB1 to promote macrophage M2 polarization. Finally, we demonstrate that BPIFB1 promotes the metastasis of hormone receptor‐positive BC by stimulating the M2‐like polarization of macrophages via the establishment of BC tumor cells/THP1 co‐culture system, qPCR, Transwell assay, and animal experiments. To our knowledge, this is the first report on the role of BPIFB1 as a tumor promoter by activating the macrophage M2 polarization in hormone receptor‐positive breast carcinoma. Together, these results provide novel insights into the mechanism of BPIFB1 in BC.
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These authors contributed equally: Anbang Hu, Yansong Liu, Hanyu Zhang
ISSN:1347-9032
1349-7006
1349-7006
DOI:10.1111/cas.15957