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HSPB1 Inhibits the Endothelial-to-Mesenchymal Transition to Suppress Pulmonary Fibrosis and Lung Tumorigenesis.

Authors
 Seo-Hyun Choi  ;  Jae-Kyung Nam  ;  Bu-Yeo Kim  ;  Junho Jang  ;  Young-Bae Jin  ;  Hae-June Lee  ;  Seungwoo Park  ;  Young Hoon Ji  ;  Jaeho Cho  ;  Yoon-Jin Lee 
Citation
 CANCER RESEARCH, Vol.76(6) : 1019-30, 2016 
Journal Title
CANCER RESEARCH
ISSN
 0008-5472 
Issue Date
2016
MeSH
Animals ; Cells, Cultured ; Disease Models, Animal ; Epithelial-Mesenchymal Transition*/radiation effects ; HSP27 Heat-Shock Proteins/analysis ; HSP27 Heat-Shock Proteins/deficiency ; HSP27 Heat-Shock Proteins/physiology* ; Heat-Shock Proteins/analysis ; Heat-Shock Proteins/physiology* ; Humans ; Janus Kinases/physiology ; Lung Neoplasms/etiology ; Lung Neoplasms/prevention & control* ; Mice ; Mice, Transgenic ; Neoplasm Proteins/analysis ; Neoplasm Proteins/physiology* ; Platelet Endothelial Cell Adhesion Molecule-1/analysis ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/prevention & control* ; STAT3 Transcription Factor/physiology
Abstract
The endothelial-to-mesenchymal transition (EndMT) contributes to cancer, fibrosis, and other pathologic processes. However, the underlying mechanisms are poorly understood. Endothelial HSP1 (HSPB1) protects against cellular stress and has been implicated in cancer progression and pulmonary fibrosis. In this study, we investigated the role of HSPB1 in mediating the EndMT during the development of pulmonary fibrosis and lung cancer. HSPB1 silencing in human pulmonary endothelial cells accelerated emergence of the fibrotic phenotype after treatment with TGFβ or other cytokines linked to pulmonary fibrosis, suggesting that HSPB1 maintains endothelial cell identity. In mice, endothelial-specific overexpression of HSPB1 was sufficient to inhibit pulmonary fibrosis by blocking the EndMT. Conversely, HSPB1 depletion in a mouse model of lung tumorigenesis induced the EndMT. In clinical specimens of non-small cell lung cancer, HSPB1 expression was absent from tumor endothelial cells undergoing the EndMT. Our results showed that HSPB1 regulated the EndMT in lung fibrosis and cancer, suggesting that HSPB1-targeted therapeutic strategies may be applicable for treating an array of fibrotic diseases.
Full Text
http://cancerres.aacrjournals.org/content/76/5/1019
DOI
10.1158/0008-5472.CAN-15-0952
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers
Yonsei Authors
Cho, Jae Ho(조재호) ORCID logo https://orcid.org/0000-0001-9966-5157
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146744
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