Mavroeidis L, Sheldon H, Briasoulis E, Marselos M, Pappas P, Harris A L
Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.
Department of Hematology, School of Medicine, University of Ioannina, University Campus, 45110 Ioannina, Greece.
Int J Oncol. 2015 Aug;47(2):455-64. doi: 10.3892/ijo.2015.3059. Epub 2015 Jun 19.
Metronomic chemotherapy is the protracted, dense administration of low sub-toxic doses of chemotherapy, to inhibit tumor angiogenesis. Vinorelbine is an orally bioavailable vinca alkaloid shown to be useable for metronomic administration. In clinical trials, metronomic vinorelbine has been demonstrated to generate sustainable antitumor efficacy at low nanomolar (nM) concentrations with negligible toxicity. We sought to determine whether the clinically relevant metronomic concentration of vinorelbine is anti-angiogenic in vitro and whether hypoxia, often induced by anti-angiogenic therapy, modifies its effectiveness. We found that the metronomic concentration of 10 nM vinorelbine inhibited human umbilical vein endothelial cell (HUVEC) proliferation, migration, tube formation and sprouting. Severe hypoxia, did not affect the inhibitory effect of metronomic vinorelbine on migration, tube formation and sprouting. However, severe hypoxia reduced its anti-proliferative effect by decreasing its ability to induce G2/M block as it shifted the cell population to the G1 phase and decreased the fraction of the cells in the DNA synthesis S phase. Furthermore, the pro-apoptotic effects of 10 nM vinorelbine were also decreased. Metronomic vinorelbine decreased the Bcl-2/Bax ratio in normoxia whereas the ratio was reduced in severe hypoxia but unaltered by vinorelbine treatment. Akt signals to an anti-apoptotic pathway and we demonstrated that the Akt inhibitor V reversed the protective effect of severe hypoxia. Thus, we provide evidence for the anti-angiogenic basis of metronomic vinorelbine and we show that severe hypoxia mediates resistance to its anti-proliferative effect on endothelial cells. Akt warrants further investigation as a potential target to circumvent this hypoxic resistance.
节拍化疗是指持续、密集地给予低亚毒性剂量的化疗药物,以抑制肿瘤血管生成。长春瑞滨是一种口服生物利用度良好的长春花生物碱,已证明可用于节拍给药。在临床试验中,节拍性长春瑞滨已被证明在低纳摩尔(nM)浓度下能产生可持续的抗肿瘤疗效,且毒性可忽略不计。我们试图确定长春瑞滨临床相关的节拍浓度在体外是否具有抗血管生成作用,以及抗血管生成治疗常诱导的缺氧是否会改变其有效性。我们发现,10 nM长春瑞滨的节拍浓度可抑制人脐静脉内皮细胞(HUVEC)的增殖、迁移、管腔形成和芽生。严重缺氧并不影响节拍性长春瑞滨对迁移、管腔形成和芽生的抑制作用。然而,严重缺氧通过降低其诱导G2/M期阻滞的能力,将细胞群体转移至G1期并减少DNA合成S期的细胞比例,从而降低了其抗增殖作用。此外,10 nM长春瑞滨的促凋亡作用也降低了。节拍性长春瑞滨在常氧条件下降低了Bcl-2/Bax比值,而在严重缺氧条件下该比值降低,但长春瑞滨治疗未改变其比值。Akt信号传导至抗凋亡途径,我们证明Akt抑制剂V可逆转严重缺氧的保护作用。因此,我们为节拍性长春瑞滨的抗血管生成基础提供了证据,并表明严重缺氧介导了其对内皮细胞抗增殖作用的抗性。Akt作为克服这种缺氧抗性的潜在靶点值得进一步研究。