Ligand independent aryl hydrocarbon receptor inhibits lung cancer cell invasion by degradation of Smad4

Highlights • Ligand-independent AhR showed tumor suppressor activity by inhibition of lung cancer cells invasion. • AhR affects the transforming growth factor-β signaling pathway by inducing Smad4 degradation by the proteasome and suppressing tumor metastasis via epithelial to mesenchymal transition...

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Veröffentlicht in:	Cancer letters 2016-07, Vol.376 (2), p.211-217
Hauptverfasser:	Lee, Chen-Chen, Yang, Wen-Hao, Li, Ching-Hao, Cheng, Yu-Wen, Tsai, Chi-Hao, Kang, Jaw-Jou
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenocarcinoma - genetics Adenocarcinoma - metabolism Adenocarcinoma - pathology Adenocarcinoma of Lung Aryl hydrocarbon receptor Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell cycle Cell growth Cell Line, Tumor Cell Movement COP9 Signalosome Complex Epithelial to mesenchymal transition Epithelial-Mesenchymal Transition Gene expression Gene Expression Regulation, Neoplastic Hematology, Oncology and Palliative Medicine Humans Inhibitor of Differentiation Protein 1 - metabolism Intracellular Signaling Peptides and Proteins - metabolism Jun-activation domain binding protein Ligands Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Metastasis Neoplasm Invasiveness Peptide Hydrolases - metabolism Phenotype Polycyclic aromatic hydrocarbons Proteasome Endopeptidase Complex - metabolism Protein expression Proteins Proteolysis Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism RNA Interference Rodents Signal Transduction Smad4 Smad4 Protein - metabolism Snail Family Transcription Factors - metabolism Studies Transcription factors Transfection Transforming growth factor-β Ubiquitination Vimentin - metabolism
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Beschreibung
Zusammenfassung:	Highlights • Ligand-independent AhR showed tumor suppressor activity by inhibition of lung cancer cells invasion. • AhR affects the transforming growth factor-β signaling pathway by inducing Smad4 degradation by the proteasome and suppressing tumor metastasis via epithelial to mesenchymal transition reduction in lung cancer cells. • AhR, Jab1, and Smad4 interacted and formed a complex that caused Smad4 ubiquitination.
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2016.03.052