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Received: 2020-02-21

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Bio-Design and Manufacturing  2020 Vol.3 No.4 P.383-395

http://doi.org/10.1007/s42242-020-00092-6


Cigarette smoke‑induced malignant transformation via STAT3 signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model


Author(s):  Wei Hou, Siyi Hu, Ken-tye Yong, Jie Zhang & Hanbin Ma

Affiliation(s):  CAS Key Laboratory of Bio-Medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, No.88 Keling Road, Huqiu District, Suzhou 215163, Jiangsu, People’s Republic of China; more

Corresponding email(s):   zjie99@jlu.edu.cn, mahb@sibet.ac.cn

Key Words:  Cigarette smoke, Microfuidic chips, STAT3, Chronic obstructive pulmonary disease


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Wei Hou, Siyi Hu, Ken-tye Yong, Jie Zhang & Hanbin Ma . Cigarette smoke‑induced malignant transformation via STAT3 signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model[J]. Journal of Zhejiang University Science D, 2020, 3(4): 383-395.

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Abstract: 
Background chronic obstructive pulmonary disease (COPD) is a severe public health problem. cigarette smoke (CS) is a risk factor for COPD and lung cancer. The underlying molecular mechanisms of CS-induced malignant transformation of bronchial epithelial cells remain unclear. In this study, we describe a lung-on-a-chip to explore the possible mechanistic link between cigarette smoke extract (CSE)-associated COPD and lung cancer. Methods An in vitro lung-on-a-chip model was used to simulate pulmonary epithelial cells and vascular endothelial cells with CSE. The levels of IL-6 and TNF-α were tested as indicators of infammation using an enzyme-linked immune sorbent assay. Apical junction complex mRNA expression was detected with qRT-PCR as the index of epithelial-to-mesenchymal transition (EMT). The efects of CSE on the phosphorylation of signal transduction and transcriptional activator 3 (STAT3) were detected by Western blotting. Flow cytometry was performed to investigate the efects of this proto-oncogene on cell cycle distribution. Results Infammation caused by CSE was achieved in a lung-on-a-chip model with a mimetic movement. CSE exposure induced the degradation of intercellular connections and triggered the EMT process. CSE exposure also activated the phosphorylation of proto-oncogene STAT3, while these efects were inhibited with HJC0152. Conclusions CSE exposure in the lung-on-a-chip model caused activation of STAT3 in epithelial cells and endothelial cells. HJC0152, an inhibitor of activated STAT3, could be a potential treatment for CS-associated COPD and lung cancer.

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