Evans David J, Wasinger Alexa M, Brey Robert N, Dunleavey James M, St Croix Brad, Bann James G
Department of Chemistry, Wichita State University, Wichita, KS, United States.
Kinesis Vaccines, LLC, Grayslake, IL, United States.
Front Oncol. 2018 Nov 6;8:506. doi: 10.3389/fonc.2018.00506. eCollection 2018.
Recent studies reveal that Seneca Valley Virus (SVV) exploits tumor endothelial marker 8 (TEM8) for cellular entry, the same surface receptor pirated by bacterial-derived anthrax toxin. This observation is particularly significant as SVV is a known oncolytic virus which selectively infects and kills tumor cells, particularly those of neuroendocrine origin. TEM8 is a transmembrane glycoprotein that is preferentially upregulated in some tumor cell and tumor-associated stromal cell populations. Both TEM8 and SVV have been evaluated for targeting of tumors of multiple origins, but the connection between the two was previously unknown. Here, we review currently understood interactions between TEM8 and SVV, anthrax protective antigen (PA), and collagen VI, a native binding partner of TEM8, with an emphasis on potential therapeutic directions moving forward.
最近的研究表明,塞内卡山谷病毒(SVV)利用肿瘤内皮标志物8(TEM8)进入细胞,该表面受体也是细菌衍生的炭疽毒素所盗用的。这一发现尤为重要,因为SVV是一种已知的溶瘤病毒,可选择性地感染并杀死肿瘤细胞,尤其是神经内分泌起源的肿瘤细胞。TEM8是一种跨膜糖蛋白,在某些肿瘤细胞和肿瘤相关基质细胞群体中优先上调。TEM8和SVV都已被评估用于靶向多种起源的肿瘤,但两者之间的联系此前并不为人所知。在此,我们综述目前所了解的TEM8与SVV、炭疽保护性抗原(PA)以及TEM8的天然结合伴侣胶原蛋白VI之间的相互作用,重点关注未来潜在的治疗方向。