Affordable Access

deepdyve-link
Publisher Website

E-cigarette promotes breast carcinoma progression and lung metastasis: Macrophage-tumor cells crosstalk and the role of CCL5 and VCAM-1.

Authors
  • Pham, Kien1
  • Huynh, Do2
  • Le, Le2
  • Delitto, Daniel3
  • Yang, Lei4
  • Huang, Jing2
  • Kang, Yibin5
  • Steinberg, Michael B6
  • Li, Jieliang2
  • Zhang, Lanjing7
  • Liu, Dongfang7
  • Tang, Moon-Shong8
  • Liu, Chen4
  • Wang, He9
  • 1 Department of Pathology, Yale School of Medicine, Yale University, New Haven, CT, USA. Electronic address: [email protected]
  • 2 Department of Pathology and Laboratory Medicine, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA.
  • 3 Department of Surgery, Johns Hopkins University School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
  • 4 Department of Pathology, Yale School of Medicine, Yale University, New Haven, CT, USA.
  • 5 Department of Molecular Biology, Princeton University, Princeton, NJ, USA.
  • 6 Department of Medicine, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA.
  • 7 Department of Pathology, Immunology & Laboratory Medicine, New Jersey Medical School, Rutgers University, Newark, NJ, USA. , (Jersey)
  • 8 Department of Environment Medicine, New York University School of Medicine, New York University, Tuxedo Park, NY, USA.
  • 9 Department of Pathology and Laboratory Medicine, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA; Department of Pathology, Immunology & Laboratory Medicine, New Jersey Medical School, Rutgers University, Newark, NJ, USA. Electronic address: [email protected] , (Jersey)
Type
Published Article
Journal
Cancer letters
Publication Date
Aug 21, 2020
Volume
491
Pages
132–145
Identifiers
DOI: 10.1016/j.canlet.2020.08.010
PMID: 32829009
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Young women represent a target of E-cigarette (E-cig) companies, raising concern for potential connections with breast cancer (BC) that have not yet been elucidated. We hypothesized that E-cig promotes BC development and lung metastasis possibly through BC-monocyte/tumor-associated macrophage (TAM) crosstalk via CCL5 and V-CAM-1 axes. We demonstrated that E-cig promoted the infiltration of circulating monocytes in mammary fat pad (MFP) model. Furthermore, E-cig exposure significantly enhanced BC cell growth in MFP tumor and metastatic lung colonization; immunohistochemical stains illustrated the increase of TAMs infiltration, reduced BC cell apoptosis and increased proliferation index after E-cig exposure. In vitro studies show E-cig vapor condensate (EVC) treatment upregulated protein expressions of CCL5, V-CAM-1, and other pro-tumorigenic factors in BC cells. Mechanistically, co-culture system demonstrated both EVC and macrophages independently stimulated BC cell growth and the migration via CCL5/CCR1/CCR5 axis. During metastasis, E-Cig exposure stimulated BC cell survival via direct interaction with infiltrated macrophages, regulated by VCAM-1 and integrin α4β1. Our findings, for the first time, showed that E-cig promotes BC growth and metastasis. This study highlights the critical role of TAMs via CCL5 and VCAM-1 pathways in E-cig promoted BC tumor development. Published by Elsevier B.V.

Report this publication

Statistics

Seen <100 times