Nuclear MET requires ARF and is inhibited by carbon nanodots through binding to phospho-tyrosine in prostate cancer

Nuclear receptor tyrosine kinases (nRTKs) are aberrantly upregulated in many types of cancers, but the regulation of nRTK remains unclear. We previously showed androgen deprivation therapy (ADT) induces nMET in castration-resistant prostate cancer (CRPC) specimens. Through gene expression microarray...

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Veröffentlicht in:	Oncogene 2019-04, Vol.38 (16), p.2967-2983
Hauptverfasser:	Xie, Yingqiu, Fan, Haiyan, Lu, Wenfu, Yang, Qing, Nurkesh, Ayan, Yeleussizov, Tleubek, Maipas, Aisulu, Lu, Jiang, Manarbek, Limara, Chen, Zhenbang, Benassi, Enrico
Format:	Artikel
Sprache:	eng
Schlagworte:	13/106 14/1 631/45 692/53 Amino acids Androgen Antagonists - pharmacology Androgen suppression therapy Androgens Androgens - metabolism Animals Apoptosis B cells Biochemistry Cancer cells Carbon Carbon - pharmacology Castration Cell Biology Cell Line, Tumor Cell Nucleus - drug effects Cell Nucleus - metabolism Complications and side effects Computer applications Crizotinib Development and progression DNA DNA damage DNA microarrays DNA repair Dosage and administration Drug resistance Gene expression Genetic research Human Genetics Humans Internal Medicine Kinases Male Medicine Medicine & Public Health Mice Mice, Knockout Oncology Phenols (Class of compounds) Phosphates Phosphorylation Prostate cancer Prostatic Neoplasms, Castration-Resistant - drug therapy Prostatic Neoplasms, Castration-Resistant - metabolism Proto-Oncogene Proteins c-met - metabolism PTEN Phosphohydrolase - metabolism PTEN protein Signal Transduction - drug effects Tyrosine Tyrosine - metabolism
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