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Lymphoma treatment is based on chemotherapy, radiotherapy, and monoclonal antibody (mAb) or other immunotherapies. The P\u2010selectin glycoprotein ligand 1 (PSGL\u20101) is expressed at the surface of hematological malignant cells and has been shown to have a pro\u2010oncogenic role in multiple myeloma and lymphoma. Here, we investigated the expression and therapeutic potential of PSGL\u20101 in T and B cell lymphomas. By flow cytometry analysis, we found that PSGL\u20101 was expressed in both T and B cell\u2010derived lymphoma cell lines but generally at higher levels in T cell lymphoma cell lines. For most T and B cell\u2010derived lymphoma cell lines, in vitro targeting with the PL1 mAb, which recognizes the PSGL\u20101 N\u2010terminal extracellular region and blocks functional interactions with selectins, resulted in reduced cell viability. The PL1 mAb pro\u2010apoptotic activity was shown to be dose\u2010dependent, to be linked to increased ERK kinase phosphorylation, and to be dependent on the MAP kinase signaling pathway. Importantly, anti\u2010PSGL\u20101 treatment of mice xenografted with the HUT\u201078 cutaneous T\u2010cell lymphoma cell line resulted in decreased tumor growth, had no effect on in vivo proliferation, but increased the levels of apoptosis in tumors. Anti\u2010PSGL\u20101 treatment of mice xenografted with a Burkitt lymphoma cell line that was resistant to anti\u2010PSGL\u20101 treatment in vitro, had no impact on tumorigenesis. These findings show that PSGL\u20101 antibody targeting triggers lymphoma cell apoptosis and substantiates PSGL\u20101 as a potential target for lymphoma therapy.<\/jats:p>","DOI":"10.1002\/hon.3257","type":"journal-article","created":{"date-parts":[[2024,2,28]],"date-time":"2024-02-28T06:24:41Z","timestamp":1709101481000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Antibody targeting of surface P\u2010selectin glycoprotein ligand 1 leads to lymphoma apoptosis and tumorigenesis inhibition"],"prefix":"10.1002","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8625-5420","authenticated-orcid":false,"given":"Jo\u00e3o L.","family":"Pereira","sequence":"first","affiliation":[{"name":"i3S\u2010Instituto de Investiga\u00e7\u00e3o e Inova\u00e7\u00e3o em Sa\u00fade da Universidade do Porto  Porto Portugal"},{"name":"IPATIMUP\u2010Institute of Molecular Pathology and Immunology of the University of Porto  Porto Portugal"},{"name":"FMUP\u2010Faculty of Medicine of the University of Porto  Porto Portugal"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Francisca","family":"Ferreira","sequence":"additional","affiliation":[{"name":"i3S\u2010Instituto de Investiga\u00e7\u00e3o e Inova\u00e7\u00e3o em Sa\u00fade da Universidade do Porto  Porto Portugal"},{"name":"IPATIMUP\u2010Institute of Molecular Pathology and Immunology of the University of Porto  Porto Portugal"},{"name":"Master\u00b4s degree in Bioengineering, ICBAS\u2010Instituto de Ci\u00eancias Biom\u00e9dicas de Abel Salazar and Faculty of Engineering University of Porto  Porto Portugal"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7347-2592","authenticated-orcid":false,"given":"Nuno R.","family":"dos Santos","sequence":"additional","affiliation":[{"name":"i3S\u2010Instituto de Investiga\u00e7\u00e3o e Inova\u00e7\u00e3o em Sa\u00fade da Universidade do Porto  Porto 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