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Cigarette smoke‑induced malignant transformation via STAT3 signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model 被引量:2
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作者 Wei Hou siyi hu +2 位作者 Ken‑tye Yong Jie Zhang Hanbin Ma 《Bio-Design and Manufacturing》 SCIE CSCD 2020年第4期383-395,共13页
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 transfor... 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-αwere tested as indicators of inflammation 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 effects 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 effects of this proto-oncogene on cell cycle distribution.Results Inflammation 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 effects 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. 展开更多
关键词 Cigarette smoke Microfluidic chips STAT3 Chronic obstructive pulmonary disease
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Preparation of chitosan-Epigallocatechin-3-O-gallate nanoparticles and their inhibitory effect on the growth of breast cancer cells 被引量:2
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作者 Yingyi Liu siyi hu +7 位作者 Yueshu Feng Peng Zou Yue Wang Pei Qin Jie Yue Yaotian Liang hui Wang Liwei Liu 《Journal of Innovative Optical Health Sciences》 SCIE EI CAS 2018年第4期43-52,共10页
In this paper,we prepared the nanoparticle drug carrier system between nanoparticles chitosan and Epigallocatechin-3 O-gallate(EGCG)for breast cancer cell inhibiting application.For this drug carrier system,chitosan a... In this paper,we prepared the nanoparticle drug carrier system between nanoparticles chitosan and Epigallocatechin-3 O-gallate(EGCG)for breast cancer cell inhibiting application.For this drug carrier system,chitosan acts as a carrier and EGOG as a drug.Which were systematically characterized and thoroughly evaluated in terms of their inhibition rate and biocompatibility.We also did a cell scratch test and the result indicated that the chitosan EGCG nanoparticles have inhibitory effect on the growth of breast cancer cells.The inhibition rate could reach up to 21.91%.This work revealed that the modification of nanopartidles paved a way for specific biomedical applications. 展开更多
关键词 Epigallocatechin-3-O gallate NANOPARTICLES inhibits tumor
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