Tumor endothelial marker 8 (TEM8)

Tumor endothelial marker 8 (TEM8), also known as Anthrax toxin receptor 1 (ANTXR1), is an integrin-like cell surface protein predominantly expressed in the tumor endothelium and, to a lesser degree, in various cancer cells[1][3]. TEM8 was first characterized as a protein upregulated in tumor vasculature compared to normal tissues and later identified as a functional receptor for anthrax toxin[1][3][5]. Its primary biological role involves modulating pathological angiogenesis—enabling the formation of new blood vessels within tumors—by interacting with extracellular matrix components and other surface receptors such as VEGFR2[1][3]. TEM8 loss leads to reduced tumor progression, angiogenesis, and metastasis in preclinical breast and colorectal cancer models, and thus TEM8 is regarded as a promising therapeutic target for cancer treatment[1][6]. In contrast to some anti-angiogenic targets, TEM8 appears dispensable for normal developmental angiogenesis, especially in knockout animal models, suggesting a therapeutic window for selective tumor targeting[3]. Additionally, TEM8 is crucial for anthrax toxin internalization but is less critical for high-affinity binding than its homolog CMG2/ANTXR2[5]. Experimental drug modalities include monoclonal antibodies and engineered protein antagonists aimed at disrupting TEM8-mediated interactions, angiogenesis, or toxin binding[3].

Other names

Anthrax toxin receptor 1ANTXR1ATR

Antibody-mediated inhibition/disruption of cell-surface TEM8 function; Competitive inhibition of anthrax toxin binding; Disruption of tumor angiogenesis and/or tumor microenvironment