【摘 要】
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Aim Head and neck cancers are the eighth most common cancer worldwide.Despite significant advances in the delivery of treatment and surgical reconstruction, the mortality rates for this disease have n
【机 构】
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Microbiology and Immunology,Virginia Commonwealth University,Richmond,VA,USA 23298;Institute of Mate
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Aim Head and neck cancers are the eighth most common cancer worldwide.Despite significant advances in the delivery of treatment and surgical reconstruction, the mortality rates for this disease have not improved in the past 4 decades.Our previous study has shown that HIV protease inhibitors (HIV PIs) induce cell apoptosis via activating endoplasmic reticulum (ER) stress.It also has been reported that a few HIV PIs are able to radiosensitize tumor cells.However, the underlying cellular mechanisms remain to be identified.The aim of this study was to examine whether HIV PIs activate the ER stress response and sensitize human head and neck carcinoma cells to radiation.Methods Human SQ20B and Fadu cells and the most commonly used HIV PIs, lopinavir and ritonavir, were used in this study.The mRNA and protein levels of ER stressrelated genes (CHOP, ATF4, XBP1, and GRP78) were detected by real time RTPCR and Western blot, respectively.Cell viability and apoptosis were analyzed using Cellometer Vision CBA.After treatment with HIV PIs, cells were irradiated at a dose of 2G or 4G.Colonies were stained and counted 10 days after irradiation.Results HIV PIs significantly induced activation of ER stress and apoptosis.Treatment of HIV PIs inhibited Akt phosphorylation, induced cell cycle arrest in G1 phase and increased tumor cell sensitivity to irradiationinduced cell death.Conclusion HIV PIs sensitize human head and neck carcinoma ceils to radiation by activating ER stress.
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