ArticleAntibodies (Basel, Switzerland)2025
Potentiating Antibody-Dependent Cellular Cytotoxicity in Triple-Negative Breast Cancer via the Humanized Anti-CD147 Antibody.
Article in Antibodies (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Fc engineering of a fully humanized anti-CD147 monoclonal antibody enhances ADCC against T-cell acute lymphoblastic leukemia and T-lymphoblastic lymphoma.Scientific reports · 2026Article
- Targeted biologics for TNBC: Advances in nanobodies, antibodies, peptides, and aptamers.Molecular therapy. Oncology · 2026Review
- Overcoming NK cell resistance in triple-negative breast cancer via adcc with a humanized anti-CD147 antibody.Cancer immunology, immunotherapy : CII · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is an aggressive subtype with high metastatic potential, poor prognosis, and the absence of estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (HER2). The lack of these receptors limits the standard treatments, such as hormone therapies and HER2-targeted antibodies like trastuzumab. These challenges highlight the critical need for novel therapeutic strategies. CD147, a transmembrane glycoprotein overexpressed in TNBC, promotes tumor progression, metastasis, and chemoresistance, making it a promising therapeutic target. This study evaluates the antibody-dependent cellular cytotoxicity (ADCC) of HuM6-1B9, a humanized anti-CD147 antibody, against MDA-MB-231 cells, a TNBC model.
methodsCFSE-labelled MDA-MB-231 cells were co-cultured with PBMCs as effector cells (E:T ratio 80:1) in the presence of HuM6-1B9 and incubated for 4 h. Cells were then collected and stained with PI, and CFSE+/PI+ dead target cells were analyzed by flow cytometry.
resultsCo-culturing MDA-MB-231 cells with peripheral blood mononuclear cells (PBMCs) in the presence of HuM6-1B9 demonstrated effective ADCC induction without direct cytotoxicity. HuM6-1B9 induced 54.01% cancer cell death via ADCC, significantly outperforming trastuzumab (26.14%) while sparing PBMCs.
conclusionThese findings support HuM6-1B9 as a prospective TNBC therapeutic and warrant further investigation into its clinical potential.
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