Effect of Cigarette Smoking on Epithelial to Mesenchymal Transition (EMT) in Lung Cancer

被引:74
|
作者
Vu, Trung [1 ]
Jin, Lin [1 ]
Datta, Pran K. [1 ]
机构
[1] Univ Alabama Birmingham, Div Hematol & Oncol, Dept Med, Ctr Comprehens Canc, Birmingham, AL 35233 USA
关键词
epithelial to mesenchymal transition; cigarette smoke; drug resistance; metastasis; and lung cancer; E-CADHERIN REPRESSION; LONG NONCODING RNA; PLASMINOGEN-ACTIVATOR; HYDROCARBON RECEPTOR; BONE METASTASIS; UP-REGULATION; STEM-CELLS; TWIST; SNAIL; CARCINOMA;
D O I
10.3390/jcm5040044
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Epithelial to mesenchymal transition (EMT) is a process that allows an epithelial cell to acquire a mesenchymal phenotype through multiple biochemical changes resulting in an increased migratory capacity. During cancer progression, EMT is found to be associated with an invasive or metastatic phenotype. In this review, we focus on the discussion of recent studies about the regulation of EMT by cigarette smoking. Various groups of active compounds found in cigarette smoke such as polycyclic aromatic hydrocarbons (PAH), nicotine-derived nitrosamine ketone (NNK), and reactive oxygen specicies (ROS) can induce EMT through different signaling pathways. The links between EMT and biological responses to cigarette smoke, such as hypoxia, inflammation, and oxidative damages, are also discussed. The effect of cigarette smoke on EMT is not only limited to cancer types directly related to smoking, such as lung cancer, but has also been found in other types of cancer. Altogether, this review emphasizes the importance of understanding molecular mechanisms of the induction of EMT by cigarette smoking and will help in identifying novel small molecules for targeting EMT induced by smoking.
引用
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页数:15
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