HER3 belongs to the epidermal growth factor receptor (EGFR) family and is known to form an active heterodimer with other three family members EGFR, HER2, and HER4. HER3 is overexpressed in lung, breast, colon, prostate, and gastric cancers. In the present study, we developed and validated an anti‑HER3 monoclonal antibody (mAb), HMab‑17 (IgG, kappa), by immunizing mice with HER3‑overexpressed CHO‑K1 cells (CHO/HER3). HMab‑17 was found to react specifically with endogenous HER3 in colorectal carcinoma cell lines, using flow cytometry. The for HMab‑17 in CHO/HER3 and Caco‑2 (a colon cancer cell line) were determined to be 3.0x10 M and 1.5x10 M via flow cytometry, respectively, suggesting high binding affinity of HMab‑17 to HER3. Then, we assessed the HMab‑17 antibody‑dependent cellular cytotoxicity (ADCC) and complement‑dependent cytotoxicity (CDC) against Caco‑2, and evaluated its antitumor capacity in a Caco‑2 xenograft model. experiments revealed HMab‑17 had strongly induced both ADCC and CDC against Caco‑2 cells. experiments on Caco‑2 xenografts revealed that HMab‑17 treatment significantly reduced tumor growth compared with the control mouse IgG. These data indicated that HMab‑17 could be a promising treatment option for HER3‑expressing colon cancers.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8261196PMC
http://dx.doi.org/10.3892/or.2021.8124DOI Listing

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