Abstract
The epidermal growth factor receptor (EGFR) contributes to tumor malignancy via gene amplification and protein overexpression. Previously, we developed an anti-human EGFR (hEGFR) monoclonal antibody, namely EMab-134, which detects hEGFR and dog EGFR (dEGFR) with high sensitivity and specificity. In this study, we produced a defucosylated mouse–dog chimeric anti-EGFR monoclonal antibody, namely E134Bf. In vitro analysis revealed that E134Bf highly exerted antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity against a canine osteosarcoma cell line (D-17) and a canine fibroblastic cell line (A-72), both of which express endogenous dEGFR. Moreover, in vivo administration of E134Bf significantly suppressed the development of D-17 and A-72 compared with the control dog IgG in mouse xenografts. These results indicate that E134Bf exerts antitumor effects against dEGFR-expressing canine cancers and could be valuable as part of an antibody treatment regimen for dogs.
Highlights
By immunizing mice with purified recombinant hEGFR ectodomain from cultures of hEGFRec-overexpressed human glioblastoma, LN229, cells, we previously developed a novel anti-human epidermal growth factor receptor (EGFR) monoclonal antibody, namely EMab134 [14]
We investigated the antitumor activities of a defucosylated mouse–dog anti-EGFR monoclonal antibody (mAb) (E134Bf) against D-17 and A-72 xenografts, both of which endogenously express dog EGFR (dEGFR)
CHO/dEGFR cells, indicating that EMab-134 crossreacts with dEGFR [16]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The epidermal growth factor receptor (EGFR) is a member of the receptor tyrosine kinases, which can form homo- or heterodimers with other EGFR family members, including HER2 (ErbB2/neu), HER3 (ErbB3), and HER4 (ErbB4) [1,2] These dimers promote cell proliferation through the activation of several signaling pathways, such as the PI3K-AKTmTOR, Ras-Raf-MEK-ERK, and JAK-STAT pathways [3]. The therapeutic measures for canine osteosarcoma include surgery, radiotherapy, and chemotherapy [12,13]. The mouse IgG2a version of EMab-134 (134-mG2a ) demonstrates antitumor activities in mouse xenograft models of hEGFR-expressing oral squamous cell carcinoma [15]. We investigated the antitumor activities of a defucosylated mouse–dog anti-EGFR mAb (E134Bf) against D-17 and A-72 xenografts, both of which endogenously express dEGFR
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