|Title:||Bortezomib enhances radiation-induced apoptosis in solid tumors by inhibiting CIP2A||Authors:||CHAO YUAN HUANG
|Issue Date:||2012||Journal Volume:||317||Journal Issue:||1||Start page/Pages:||9-15||Source:||Cancer Letters||Abstract:||
Previously, we demonstrated that cancerous inhibitor of protein phosphatase 2A (CIP2A) mediates bortezomib-induced apoptosis in hepatocellular carcinoma cells. Herein, we report that bortezomib sensitizes solid tumor cells to radiation-induced apoptosis. Treatment with a combination of bortezomib and radiation downregulated CIP2A in a dose-dependent manner in solid tumor cells. Knockdown of CIP2A enhanced radiation-induced apoptosis in cancer cells, and ectopic expression of CIP2A in cancer cells abolished radiation-induced apoptosis. Finally, our in vivo data showed that bortezomib and radiation combination treatment decreased tumor growth significantly. Thus, bortezomib sensitized solid tumor cells to radiation through the inhibition of CIP2A. ? 2011 Elsevier Ireland Ltd.
|ISSN:||0304-3835||DOI:||10.1016/j.canlet.2011.11.005||SDG/Keyword:||bortezomib; phosphoprotein phosphatase 2A; animal experiment; animal model; animal tissue; antineoplastic activity; apoptosis; article; cancer cell; cancer radiotherapy; controlled study; DNA fragmentation; down regulation; drug efficacy; drug safety; enzyme inhibition; flow cytometry; human; human cell; in vitro study; in vivo study; liver cell carcinoma; male; mouse; nonhuman; priority journal; protein phosphorylation; radiosensitivity; solid tumor; treatment response; tumor xenograft; uterine cervix cancer; Animals; Apoptosis; Autoantigens; Boronic Acids; Cell Line, Tumor; Chemoradiotherapy; Dose-Response Relationship, Drug; Down-Regulation; Humans; Male; Membrane Proteins; Mice; Mice, Nude; Neoplasms, Experimental; Pyrazines; Radiation-Sensitizing Agents; RNA Interference; Time Factors; Transfection; Tumor Burden; Xenograft Model Antitumor Assays
|Appears in Collections:||食品安全與健康研究所|
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.