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首页> 外文期刊>International Journal of Molecular Sciences >Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells
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Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells

机译：磺酰色基 - 4-α（CHW09）和紫外-c（UVC）的组合处理可增强增殖抑制，凋亡，氧化应激和对口腔癌细胞的DNA损伤

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The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously developed sulfonyl chromen-4-ones (CHW09), namely UVC/CHW09. Cell viability, apoptosis, oxidative stress, and DNA damage for the individual and combined treatments for UVC and/or CHW09 were examined in oral cancer Ca9-22 cells. In 24 h MTS assay, UVC (30 J/m 2 ; UVC30), or CHW09 (25 and 50 μg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2’-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy.
机译：到目前为止，尚未全面研究了铬源衍生化合物对UVC诱导的增殖抑制的敏化作用。本研究的主题是在使用先前显影的磺酰化铬-4-α（CHW09），即UVC / CHW09的同时检查口腔癌细胞的增殖变化。使用UVC（254nm），即UVC / CHW09。在口服癌细胞CA9-22细胞中检测细胞活力，细胞凋亡，氧化应激和用于UVC和/或CHW09的组合治疗的DNA损伤。在24小时MTS测定中，UVC（30J / m 2; UVC30），或CHW09（25和50μg/ ml;即，CHW09-25和CHW09-50）显示54％，59％和45％的活力。组合治疗（UVC30 / CHW09-25和UVC30 / CHW09-50）显示出较低的细胞活力（45％和35％）。机械地，UVC / CHW09诱导比个体治疗和未处理的对照诱导更高的凋亡，其通过对SubG1，annexin V / 7-氨基酰胺霉素D，Pancaspase和Caspases 3/7活性的流式细胞术的证据支持，以及用于切割聚的蛋白质印迹（ ADP-核糖）聚合酶。此外，该切割的PARP表达由Pancaspase抑制剂Z-VAD-FMK下调。 UVC / CHW09表现出比单个治疗和未处理的对照在流式细胞术方面具有更高的氧化应激，用于反应性氧物种，线粒体膜电位和线粒体质量。此外，UVC / CHW09显示出比单个处理和未处理的对照对H2A组蛋白家族构件X和8-氧代-2'-脱氧胍的流式细胞术而言的较高的DNA损伤。总之，联合治疗UVC / CHW09抑制增殖，促进口腔癌细胞的凋亡，氧化应激和DNA损伤，提供了一种新的磺酰基染色-4-β-抑制uVC诱导的口腔癌治疗的增殖抑制。

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