Effect of gemcitabine on the expression of apoptosis-related genes in human pancreatic cancer cells
Autor: | Norio Sawabu, Toshinari Minamoto, Pei-Hong Jiang, Yoshiharu Motoo |
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Jazyk: | angličtina |
Rok vydání: | 2006 |
Předmět: |
Apoptosis related genes
PANC-1 Antimetabolites Antineoplastic Apoptosis Pancreatitis-Associated Proteins DNA Fragmentation Biology Deoxycytidine Glycogen Synthase Kinase 3 Antigens Neoplasm Clinical Research Cell Line Tumor Pancreatic cancer Biomarkers Tumor medicine Humans Lectins C-Type Pancreatitis-associated protein RNA Messenger Gene Heat-Shock Proteins Cell Proliferation Glycogen Synthase Kinase 3 beta GSK-3β Gastroenterology TP53INPI DNA Neoplasm General Medicine medicine.disease Molecular biology Gemcitabine Gene Expression Regulation Neoplastic Pancreatic Neoplasms Cancer research Apoptosis Regulatory Proteins Carrier Proteins medicine.drug |
Zdroj: | World Journal of Gastroenterology. 12(10):1597-1602 |
ISSN: | 1007-9327 |
Popis: | 金沢大学がん研究所 Aim: To investigate the expression of genes involved in the gemcitabine-induced cytotoxicity in human pancreatic cancer cells. Methods: A human pancreatic cancer cell line, PANC-1, was cultured. 1 × 104 PANC-1 cells were plated in 96-well microtiter plates. After being incubated for 24 h, gemcitabine was added to the medium at concentrations ranging 2.5 -1 000 mg/L. The AlamarBlue dye method was used for cell growth analysis. DNA fragmentation was quantitatively assayed using a DNA fragmentation enzyme-linked immunosorbent assay (ELISA) kit. PAP and TP53INP1 mRNA expression was determined using the reverse transcription-polymerase chain reaction with semi-quantitative analysis. The expression of GSK-3β and phospho-GSK-3β proteins was examined with Western blot analysis. Results: The IC50 for the drug after a 48-h exposure to gemcitabine was 16 mg/L. The growth of PANC-1 cells was inhibited by gemcitabine in a concentration-dependent manner (P< 0.0001) and the cell growth was also inhibited throughout the time course (P |
Databáze: | OpenAIRE |
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