Enhancement of cytotoxic effects of gemcitabine by Dclk1 inhibition through suppression of Chk1 phosphorylation in human pancreatic cancer cells

Although gemcitabine (GEM) is frequently used in the treatment of pancreatic cancer, the effects are limited. To increase the inhibitory effect of GEM, the identification of a molecular target is needed. Recent studies have revealed that doublecortin-like kinase 1 (Dclk1) positively regulates tumor...

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Veröffentlicht in:	Oncology reports 2017-11, Vol.38 (5), p.3238-3244
Hauptverfasser:	Kawamura, Daichi, Takemoto, Yoshihiro, Nishimoto, Arata, Ueno, Koji, Hosoyama, Tohru, Shirasawa, Bungo, Tanaka, Toshiki, Kugimiya, Naruji, Harada, Eijiro, Hamano, Kimikazu
Format:	Artikel
Sprache:	eng
Schlagworte:	Apoptosis Apoptosis - drug effects Ataxia Telangiectasia Mutated Proteins - genetics Benzodiazepinones - administration & dosage Cell cycle Cell Cycle Checkpoints - drug effects Cell Line, Tumor Cell Proliferation - drug effects Checkpoint Kinase 1 - genetics Chk1 Dclk1 Deoxycytidine - administration & dosage Deoxycytidine - analogs & derivatives Deoxyribonucleic acid Development and progression DNA DNA damage DNA repair inhibition Drug therapy Epithelial-Mesenchymal Transition - drug effects Gemcitabine Gene expression Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Health aspects Humans Immunoglobulins Innovations Intracellular Signaling Peptides and Proteins - antagonists & inhibitors Intracellular Signaling Peptides and Proteins - genetics Kinases Molecular targeted therapy Neoplasm Proteins - genetics Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Patient outcomes Phosphorylation Phosphotransferases Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - genetics Proteins Pyrimidines - administration & dosage Signal Transduction - drug effects
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