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HIV protease inhibitors sensitize human head and neck carcinoma cells to radiation by activating endoplasmic reticulum stress

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中国药理学通报 2015年第B11期31卷 233-233页

作者： LIURun-ping ZHUANGXiao-suan WANGXiang RossMikkelsen ZHOUHui-ping microbilogyandimmunology VirginiaCommonwealthUniversityRichmondVAUSA223298

Aim Head and neck cancers are the eighth most common cancer worldwide. Despite significant ad- vances 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 radio- sensitize 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 ritona- vir, were used in this study. The mRNA and protein levels of ER stress-related genes （ CHOP, ATF4, XBP-1, and GRP78 ） were detected by real time RT-PCR and Western blot, respectively. Cell viability and apoptosis were ana- lyzed using Cellometer Vision CBA. After treatment with HIV PIs, cells were irradiated at a dose of 2G or 4G. Col- onies 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 irradiation-induced cell death. Conclusion HIV PIs sensitize human head and neck carcinoma cells to radiation by activating ER stress.

关键词： HIV protease inhibitors head and neck carcinoma ER stress akt signaling pathway cell cycle arrest

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