Nutlin-3 inhibits epithelial–mesenchymal transition by interfering with canonical transforming growth factor-β1-Smad-Snail/Slug axis

Nutlin-3 inhibits epithelial–mesenchymal transition by interfering with canonical transforming growth factor-β1-Smad-Snail/Slug axis

Highlights • EMT caused by TGF-β1 could be inhibited by Nutlin-3 in p53-null tumor cells. • The mechanism relies on the prohibitive effect of Nutlin-3 on Smads pathway. • Nutlin-3 exhibited noticeable suppressive activity against cell migration. • EGFRIs could be sensitized by combination with Nutli...

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Veröffentlicht in:Cancer letters 2014-01, Vol.342 (1), p.82-91
Hauptverfasser: Wu, Yeping, Fu, Yingying, Zheng, Lin, Lin, Guanyu, Ma, Jian, Lou, Jianshu, Zhu, Hong, He, Qiaojun, Yang, Bo
Format: Artikel
Sprache:eng
Schlagworte:
Antineoplastic Agents - pharmacology
Cadherins - genetics
Cadherins - metabolism
Cell Line, Tumor
Cell Movement - drug effects
Drug Evaluation, Preclinical
Drug Synergism
EMT
Epithelial-Mesenchymal Transition - drug effects
Gene Expression - drug effects
Hematology, Oncology and Palliative Medicine
Humans
Imidazoles - pharmacology
Nutlin-3
Phosphorylation
Piperazines - pharmacology
Protein Kinase Inhibitors - pharmacology
Protein Processing, Post-Translational
Quinazolines - pharmacology
Receptor, Epidermal Growth Factor - antagonists & inhibitors
RNA, Messenger - genetics
RNA, Messenger - metabolism
Signal Transduction - drug effects
Smad pathway
Smad Proteins - metabolism
Snail Family Transcription Factors
TGF-β1
Transcription Factors - metabolism
Transforming Growth Factor beta1 - physiology
Up-Regulation
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Beschreibung
Zusammenfassung:Highlights • EMT caused by TGF-β1 could be inhibited by Nutlin-3 in p53-null tumor cells. • The mechanism relies on the prohibitive effect of Nutlin-3 on Smads pathway. • Nutlin-3 exhibited noticeable suppressive activity against cell migration. • EGFRIs could be sensitized by combination with Nutlin-3 with TGF-β1 treatment.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2013.08.039