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Radiosensitization of Head and Neck Squamous Cell Carcinoma (HNSCC) by a Podophyllotoxin.
ACS Medicinal Chemistry Letters ( IF 3.5 ) Pub Date : 2019-07-23 , DOI: 10.1021/acsmedchemlett.9b00270 Angel Resendez 1 , Dhanir Tailor 1 , Edward Graves 1, 2 , Sanjay V Malhotra 1, 2
ACS Medicinal Chemistry Letters ( IF 3.5 ) Pub Date : 2019-07-23 , DOI: 10.1021/acsmedchemlett.9b00270 Angel Resendez 1 , Dhanir Tailor 1 , Edward Graves 1, 2 , Sanjay V Malhotra 1, 2
Affiliation
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Surgical resection and radiotherapy are an effective treatment in many head and neck squamous cell carcinomas (HNSCC), but in others, the development of radiotherapy resistance limits treatment efficacy and permits disease progression. We developed a novel multiwell radiation dosing method to increase the throughput of our investigation of the activity of a novel podophyllotoxin SU093 in acting as a radiosensitizer in the HNSCC models FaDu and SCC-25. These in vitro studies showed that combining SU093 with 5 Grays ionizing radiation acted synergistically to increase HNSCC apoptosis and decrease its proliferation via inhibition of Nuclear factor, erythroid 2 like 2 (Nrf2), a key effector of the DNA damage response induced by ionizing radiation. Combined treatment reduced in vitro migration in a simulated wounding model while also promoting cell cycle arrest at the G2/M phase. These findings validate the potential of SU093 as a synergistic radiosensitizing agent for use in combination with localized radiotherapy in treatment resistant HNSCC.
中文翻译：
鬼臼毒素对头颈部鳞状细胞癌（HNSCC）的放射增敏作用。
手术切除和放疗是许多头颈鳞状细胞癌（HNSCC）的有效治疗方法，但在其他情况下，放疗抗性的发展限制了治疗效果并允许疾病进展。我们开发了一种新颖的多孔辐射定量给药方法，以增加我们对新型鬼臼毒素SU093在HNSCC模型FaDu和SCC-25中充当放射增敏剂的活性的研究通量。这些体外研究表明，将SU093与5 Grays电离辐射组合使用可协同发挥作用，通过抑制核因子类红细胞2样2（Nrf2）抑制HNSCC细胞凋亡，并降低其增殖，NRF2是电离辐射诱导的DNA损伤反应的关键效应子。联合处理减少了模拟创伤模型中的体外迁移，同时还促进了G2 / M期的细胞周期停滞。这些发现证实了SU093作为协同放射增敏剂与局部放疗联合用于治疗性HNSCC的潜力。
更新日期：2019-08-08
中文翻译：
鬼臼毒素对头颈部鳞状细胞癌（HNSCC）的放射增敏作用。
手术切除和放疗是许多头颈鳞状细胞癌（HNSCC）的有效治疗方法，但在其他情况下，放疗抗性的发展限制了治疗效果并允许疾病进展。我们开发了一种新颖的多孔辐射定量给药方法，以增加我们对新型鬼臼毒素SU093在HNSCC模型FaDu和SCC-25中充当放射增敏剂的活性的研究通量。这些体外研究表明，将SU093与5 Grays电离辐射组合使用可协同发挥作用，通过抑制核因子类红细胞2样2（Nrf2）抑制HNSCC细胞凋亡，并降低其增殖，NRF2是电离辐射诱导的DNA损伤反应的关键效应子。联合处理减少了模拟创伤模型中的体外迁移，同时还促进了G2 / M期的细胞周期停滞。这些发现证实了SU093作为协同放射增敏剂与局部放疗联合用于治疗性HNSCC的潜力。
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