Decitabine inhibits the cell growth of cholangiocarcinoma in cultured cell lines and mouse xenografts
| Autor: | Hongbo Li, Shun-chang Zhou, Bing Wang, Rui Yang, Shengquan Zou |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
autophagy
Cancer Research Pathology medicine.medical_specialty Cell cycle checkpoint Cell Decitabine Biology Flow cytometry chemistry.chemical_compound medicine Propidium iodide medicine.diagnostic_test Cell growth apoptosis Articles Cell cycle medicine.anatomical_structure Oncology chemistry Apoptosis Cancer research cell cycle cholangiocarcinoma decitabine medicine.drug |
| Zdroj: | Oncology Letters |
| ISSN: | 1792-1082 1792-1074 |
| DOI: | 10.3892/ol.2014.2499 |
| Popis: | Decitabine (DAC), an inhibitor of DNA methyltransferase, demonstrates antitumor activities in various types of cancer. However, its therapeutic potential for cholangiocarcinoma (CCA), one of the most aggressive gastrointestinal malignancies, remains to be explored. The present study investigated the antiproliferative effects of DAC on CCA cells in vitro and in vivo. Human CCA cell lines, TFK-1 and QBC939, were used as models to investigate DAC on the cell growth and proliferation of CCA. Cell proliferation was evaluated by Cell Counting Kit-8 assay combined with clonogenic survival assay. Flow cytometry, Hoechst 33342/propidium iodide staining and green fluorescent protein-tagged MAP-LC3 detection were applied to determine cell cycle progression, apoptosis and autophagy. Nude mice with TFK-1 xenografts were evaluated for tumor growth following DAC treatment. DAC was observed to significantly suppress the proliferation of cultured TFK-1 and QBC939 cells, accompanied with enhanced apoptosis, autophagy and cell cycle arrest at G2/M phase. In TFK-1 mouse xenografts, DAC retarded the tumor growth and increased the survival of CCA tumor-bearing mice. |
| Databáze: | OpenAIRE |
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