Proapoptotic Activation of Death Receptor 5 on Tumor Endothelial Cells Disrupts the Vasculature and Reduces Tumor Growth

WilsonN.S.; YangA.; YangB.; CoutoS.; SternH.; GogineniA.; PittiR.; MarstersS.; WeimerR.M.; SinghM.; AshkenaziA.

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Proapoptotic Activation of Death Receptor 5 on Tumor Endothelial Cells Disrupts the Vasculature and Reduces Tumor Growth

机译：肿瘤内皮细胞上死亡受体5的促凋亡激活破坏了血管，降低了肿瘤的生长

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The proapoptotic death receptor DR5 has been studied extensively in cancer cells, but its action in the tumor microenvironment is not well defined. Here, we uncover a role for DR5 signaling in tumor endothelial cells (ECs). We detected DR5 expression in ECs within tumors but not normal tissues. Treatment of tumor-bearing mice with an oligomeric form of the DR5 ligand Apo2L/TRAIL induced apoptosis in tumor ECs, collapsing blood vessels and reducing tumor growth: Vascular disruption and antitumor activity required DR5 expression on tumor ECs but not malignant cells. These results establish a therapeutic paradigm for proapoptotic receptor agonists as selective tumor vascular disruption agents, providing an alternative, perhaps complementary, strategy to their use as activators of apoptosis in malignant cells.

机译：凋亡前死亡受体DR5已在癌细胞中进行了广泛研究，但其在肿瘤微环境中的作用尚不明确。在这里，我们发现DR5信号在肿瘤内皮细胞（EC）中的作用。我们在肿瘤而非正常组织内的EC中检测到DR5表达。用DR5配体Apo2L / TRAIL的低聚形式治疗荷瘤小鼠会诱导肿瘤EC凋亡，塌陷血管并减少肿瘤生长：血管破裂和抗肿瘤活性需要DR5在肿瘤EC上表达，而不是恶性细胞。这些结果建立了促凋亡受体激动剂作为选择性肿瘤血管破坏剂的治疗范例，为它们用作恶性细胞凋亡激活剂提供了一种替代的，可能是互补的策略。

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《Cancer Cell》 |2012年第1期|共11页
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WilsonN.S.; YangA.; YangB.; CoutoS.; SternH.; GogineniA.; PittiR.; MarstersS.; WeimerR.M.; SinghM.; AshkenaziA.;
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正文语种 eng
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专利

1. Proapoptotic Activation of Death Receptor 5 on Tumor Endothelial Cells Disrupts the Vasculature and Reduces Tumor Growth [J] . WilsonN.S., YangA., YangB., Cancer Cell . 2012,第1期

机译：肿瘤内皮细胞上死亡受体5的促凋亡激活破坏了血管，降低了肿瘤的生长
2. Vascular endothelial growth factor receptor 2 inhibition in-vivo affects tumor vasculature in a tumor type-dependent way and downregulates vascular endothelial growth factor receptor 2 protein without a prominent role for miR-296. [J] . Langenkamp E, Zwiers PJ, Moorlag HE, Anti-cancer drugs . 2012,第2期

机译：体内血管内皮生长因子受体2抑制以肿瘤类型依赖性的方式影响肿瘤脉管系统，并下调血管内皮生长因子受体2蛋白，而miR-296没有明显作用。
3. Tumor Necrosis Factor Induces Tumor Necrosis via Tumor Necrosis Factor Receptor Type 1-Expressing Endothelial Cells of the Tumor Vasculature [J] . Benjamin Stoelcker, Brigitte Ruhland, Thomas Hehlgans, American Journal of Pathology . 2000,第4期

机译：肿瘤坏死因子通过表达肿瘤血管的肿瘤坏死因子受体1型内皮细胞诱导肿瘤坏死。
4. ~(123)I-Vascular Endothelial Growth Factor165 (~(123)I-VEGF_(165)) Binding Sites in Tumor Cells: Implication for Tumor Scintigraphy [C] . S.R. Li, C. Bischof, S. Kapiotis, NATO Advanced Study Institute on Vascular Endothelium : Mechanisms of Cell Signaling . 1999

机译：〜（123）I-血管内皮生长因子165（〜（123）I-VEGF_（165））肿瘤细胞中的结合位点：肿瘤闪烁的含义
5. Molecular studies on tumor cell-vasculature interactions: Adhesion molecules, endothelial cell retraction, tumor cell spreading, and modulatory role of eicosanoid 12(S)-HETE. [D] . Tang, Dean Guo. 1994

机译：肿瘤细胞与血管系统相互作用的分子研究：粘附分子，内皮细胞收缩，肿瘤细胞扩散和类花生酸12（S）-HETE的调节作用。
6. Destruction of tumor vasculature and abated tumor growth upon VEGF blockade is driven by proapoptotic protein Bim in endothelial cells [O] . Edwina Naik, Lorraine A. OReilly, Marie-Liesse Asselin-Labat, 2011

机译：内皮细胞中的凋亡蛋白Bim驱动着VEGF阻断后肿瘤脉管系统的破坏和肿瘤生长的减弱
7. Proapoptotic Activation of Death Receptor 5 on Tumor Endothelial Cells Disrupts the Vasculature and Reduces Tumor Growth [O] . Wilson Nicholas S., Yang Annie, Yang Becky, 2012

机译：肿瘤内皮细胞上死亡受体5的促凋亡激活破坏了血管，降低了肿瘤的生长

Proapoptotic Activation of Death Receptor 5 on Tumor Endothelial Cells Disrupts the Vasculature and Reduces Tumor Growth

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