Posttranscriptional silencing of the lncRNA MALAT1 by miR-217 inhibits the epithelial–mesenchymal transition via enhancer of zeste homolog 2 in the malignant transformation of HBE cells induced by cigarette smoke extract

Lung cancer is regarded as the leading cause of cancer-related deaths, and cigarette smoking is one of the strongest risk factors for the development of lung cancer. However, the mechanisms for cigarette smoke-induced lung carcinogenesis remain unclear. The present study investigated the effects of...

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Veröffentlicht in:	Toxicology and applied pharmacology 2015-12, Vol.289 (2), p.276-285
Hauptverfasser:	Lu, Lu, Luo, Fei, Liu, Yi, Liu, Xinlu, Shi, Le, Lu, Xiaolin, Liu, Qizhan
Format:	Artikel
Sprache:	eng
Schlagworte:	60 APPLIED LIFE SCIENCES Bronchi - drug effects Bronchi - metabolism Bronchi - pathology CARCINOGENESIS Cell Line, Transformed Cell Transformation, Neoplastic - chemically induced Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology CHRONIC EXPOSURE Cigarette smoke extract (CSE) DEATH Dose-Response Relationship, Drug Enhancer of Zeste Homolog 2 Protein Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Epithelial-Mesenchymal Transition - drug effects Epithelial–mesenchymal transition (EMT) Gene Expression Regulation, Neoplastic HAZARDS Histone Demethylases - metabolism Histones - metabolism Humans lncRNAs Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Lung Neoplasms - prevention & control LUNGS MicroRNAs - genetics MicroRNAs - metabolism miRNAs MORPHOLOGY NEOPLASMS Polycomb Repressive Complex 2 - genetics Polycomb Repressive Complex 2 - metabolism RNA Interference RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction - drug effects Smoke - adverse effects Smoking - adverse effects Time Factors TOBACCO PRODUCTS TOBACCO SMOKES Transfection TRANSFORMATIONS
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