Department of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia, PA.
Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Photochem Photobiol. 2020 Mar;96(2):358-364. doi: 10.1111/php.13187. Epub 2019 Dec 17.
Photodynamic therapy (PDT) with photosensitizer verteporfin is a clinically approved vascular disrupting modality that is currently in clinical trial for cancer treatment. In this study, we evaluated PDT in combination with either mTORC1 inhibitor rapamycin or mTORC1/C2 dual inhibitor AZD2014 for therapeutic enhancement in SVEC endothelial cells. Verteporfin-PDT alone induced cell apoptosis by activating the intrinsic apoptotic pathway. However, it increased the expression of anti-apoptotic protein MCL-1 and the phosphorylation of S6, a downstream molecule of mTOR signaling. In contrast, mTOR inhibitors rapamycin and AZD2014 did not induce apoptosis in SVEC cells. They suppressed MCL-1 expression and S6 phosphorylation and imposed a potent inhibition on cell proliferation. PDT in combination with mTOR inhibitors activated the intrinsic apoptotic pathway and resulted in increased apoptosis. Combination treatments also led to sustained inhibition of cell proliferation. Although AZD2014 was more effective for cell growth inhibition and PDT enhancement than rapamycin at the higher concentrations examined in the study, both inhibitors effectively enhanced PDT response, suggesting that inhibition of mTORC1 is crucial for PDT enhancement. Our results indicate that mTOR inhibitors mechanistically cooperate with PDT for enhanced cell death and sustained growth inhibition, supporting a combination approach for therapeutic enhancement.
光动力疗法(PDT)联合光敏剂维替泊芬是一种临床批准的血管破坏模式,目前正在临床试验中用于癌症治疗。在这项研究中,我们评估了 PDT 联合 mTORC1 抑制剂雷帕霉素或 mTORC1/C2 双重抑制剂 AZD2014 对 SVEC 内皮细胞治疗增强的作用。维替泊芬-PDT 通过激活内在凋亡途径单独诱导细胞凋亡。然而,它增加了抗凋亡蛋白 MCL-1 的表达和 mTOR 信号下游分子 S6 的磷酸化。相比之下,mTOR 抑制剂雷帕霉素和 AZD2014 不会诱导 SVEC 细胞凋亡。它们抑制 MCL-1 表达和 S6 磷酸化,并对细胞增殖产生强烈抑制作用。PDT 联合 mTOR 抑制剂激活内在凋亡途径,导致细胞凋亡增加。联合治疗还导致细胞增殖持续抑制。尽管在研究中检查的较高浓度下,AZD2014 比雷帕霉素更有效地抑制细胞生长和增强 PDT,但两种抑制剂都有效地增强了 PDT 反应,表明抑制 mTORC1 对于增强 PDT 至关重要。我们的结果表明,mTOR 抑制剂在机制上与 PDT 协同作用以增强细胞死亡和持续的生长抑制,支持联合治疗方法以增强治疗效果。