Pristimerin causes G1 arrest, induces apoptosis, and enhances the chemosensitivity to gemcitabine in pancreatic cancer cells

Despite rapid advances in chemotherapy and surgical resection strategies, pancreatic cancer remains the fourth leading cause of cancer related deaths in the United States with a 5-year survival rate of less than 5%. Therefore, novel therapeutic agents for the prevention and treatment of pancreatic c...

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Veröffentlicht in:	PloS one 2012-08, Vol.7 (8), p.e43826
Hauptverfasser:	Wang, Yongwei, Zhou, Yinan, Zhou, Haoxin, Jia, Guang, Liu, Ji, Han, Bing, Cheng, Zhuoxin, Jiang, Hongchi, Pan, Shangha, Sun, Bei
Format:	Artikel
Sprache:	eng
Schlagworte:	Anticarcinogenic Agents - pharmacology Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Bcl-2 protein Binding Biology Cancer Cancer cells Cancer therapies Care and treatment Caspase Caspase-3 Cell cycle Cell death Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Cell Survival - drug effects Chemical compounds Chemotherapy Complications and side effects Cyclin-dependent kinase 2 Cyclin-dependent kinase 4 Cyclin-dependent kinase inhibitor p21 Cyclin-dependent kinase inhibitor p27 Cyclins Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology Deoxyribonucleic acid DNA DNA - metabolism Dosage and administration Drug Synergism Drug therapy G1 Phase Cell Cycle Checkpoints - drug effects Gemcitabine Genetic aspects Growth inhibition Health aspects Humans Inhibition Kinases Medical prognosis Medicine NF-kappa B - metabolism NF-κB protein Pancreatic cancer Pancreatic Neoplasms - pathology Pharmacology Physiological aspects Prostate Protein Transport - drug effects Proteins Proto-Oncogene Proteins c-bcl-2 - metabolism Surgery Transcription Translocation Triterpenes - pharmacology
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