CLC number:
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2020-08-29
Cited: 0
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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.
@article{title="Cigarette smoke‑induced malignant transformation via STAT3
signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model",
author="Wei Hou, Siyi Hu, Ken-tye Yong, Jie Zhang & Hanbin Ma ",
journal="Journal of Zhejiang University Science D",
volume="3",
number="4",
pages="383-395",
year="2020",
publisher="Zhejiang University Press & Springer",
doi="10.1007/s42242-020-00092-6"
}
%0 Journal Article
%T Cigarette smoke‑induced malignant transformation via STAT3
signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model
%A Wei Hou
%A Siyi Hu
%A Ken-tye Yong
%A Jie Zhang & Hanbin Ma
%J Journal of Zhejiang University SCIENCE D
%V 3
%N 4
%P 383-395
%@ 1869-1951
%D 2020
%I Zhejiang University Press & Springer
%DOI 10.1007/s42242-020-00092-6
TY - JOUR
T1 - Cigarette smoke‑induced malignant transformation via STAT3
signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model
A1 - Wei Hou
A1 - Siyi Hu
A1 - Ken-tye Yong
A1 - Jie Zhang & Hanbin Ma
J0 - Journal of Zhejiang University Science D
VL - 3
IS - 4
SP - 383
EP - 395
%@ 1869-1951
Y1 - 2020
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1007/s42242-020-00092-6
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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