Head & neck · 2015
Regulation of tumor progression via the Snail-RKIP signaling pathway by nicotine exposure in head and neck squamous cell carcinoma.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Nieh Shin, Jao Shu-Wen, Yang Chin-Yuh, Lin Yaoh-Shiang, Tseng Yi-Han, Liu Chia-Lin, Lee Tsai-Yu, Liu Tsung-Yun, Chu Yueng-Hsiang, Chen Su-Feng
Аннотация
BACKGROUND: Recent studies suggest that long-term exposure of the carcinogen 4-methylnitrosamino-1-3-pyridyl-1-butanone (NNK) found in tobacco smoke is involved in the progression of head and neck squamous cell carcinoma (HNSCC). The underlying nicotine-mediated mechanism remains unclear.
METHODS: An analysis of SCC-25 and Fadu cells with or without NNK exposure focusing on the evaluation of migration and invasion abilities, the expression of epithelial-mesenchymal transition, drug-resistance-related genes, properties of cancer stem cells (CSCs), and anti-apoptosis was performed.
RESULTS: Long-term NNK exposure enhances migration and invasion with morphological alterations in a dose-dependently manner. Furthermore, NNK exposure also upregulates Snail, promotes sphere-forming ability, and overexpresses aldehyde dehydrogenase 1 (ALDH1), Nanog, OCT4, ABCG2, and MDR1.
CONCLUSION: The current study confirmed that long-term NNK exposure plays a role in HNSCC by increasing anti-apoptosis and therapeutic resistance via the Snail-RKIP signaling pathway. Our data also suggest that α7 nicotinic acetylcholine receptor (α7-nAChR) inhibition or targeting Snail may provide a feasible rationale for preventing the progression of HNSCC.
METHODS: An analysis of SCC-25 and Fadu cells with or without NNK exposure focusing on the evaluation of migration and invasion abilities, the expression of epithelial-mesenchymal transition, drug-resistance-related genes, properties of cancer stem cells (CSCs), and anti-apoptosis was performed.
RESULTS: Long-term NNK exposure enhances migration and invasion with morphological alterations in a dose-dependently manner. Furthermore, NNK exposure also upregulates Snail, promotes sphere-forming ability, and overexpresses aldehyde dehydrogenase 1 (ALDH1), Nanog, OCT4, ABCG2, and MDR1.
CONCLUSION: The current study confirmed that long-term NNK exposure plays a role in HNSCC by increasing anti-apoptosis and therapeutic resistance via the Snail-RKIP signaling pathway. Our data also suggest that α7 nicotinic acetylcholine receptor (α7-nAChR) inhibition or targeting Snail may provide a feasible rationale for preventing the progression of HNSCC.
Предметные рубрики MeSH
Aldehyde Dehydrogenase 1 FamilyApoptosisCarcinogensCarcinoma, Squamous CellCell Culture TechniquesCell Line, TumorCell MovementDisease ProgressionDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHead and Neck NeoplasmsHumansHypopharyngeal NeoplasmsIsoenzymesMouth NeoplasmsNeoplasm InvasivenessNeoplasm StagingNeoplastic Stem CellsNicotineNicotinic AgonistsNitrosaminesRetinal DehydrogenaseSignal TransductionSnail Family Transcription FactorsTongue NeoplasmsTranscription FactorsUp-Regulationalpha7 Nicotinic Acetylcholine Receptor