{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T17:41:15Z","timestamp":1793209275983,"version":"4.5.0"},"reference-count":46,"publisher":"American Society of Hematology","issue":"22","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,11,30]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The use of Bruton tyrosine kinase inhibitors, such as ibrutinib, to block B-cell receptor signaling has achieved a remarkable clinical response in several B-cell malignancies, including mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL). Acquired drug resistance, however, is significant and affects the long-term survival of these patients. Here, we demonstrate that the transcription factor early growth response gene 1 (EGR1) is involved in ibrutinib resistance. We found that EGR1 expression is elevated in ibrutinib-resistant activated B-cell\u2013like subtype DLBCL and MCL cells and can be further upregulated upon ibrutinib treatment. Genetic and pharmacological analyses revealed that overexpressed EGR1 mediates ibrutinib resistance. Mechanistically, TCF4 and EGR1 self-regulation induce EGR1 overexpression that mediates metabolic reprogramming to oxidative phosphorylation (OXPHOS) through the transcriptional activation of PDP1, a phosphatase that dephosphorylates and activates the E1 component of the large pyruvate dehydrogenase complex. Therefore, EGR1-mediated PDP1 activation increases intracellular adenosine triphosphate production, leading to sufficient energy to enhance the proliferation and survival of ibrutinib-resistant lymphoma cells. Finally, we demonstrate that targeting OXPHOS with metformin or IM156, a newly developed OXPHOS inhibitor, inhibits the growth of ibrutinib-resistant lymphoma cells both in\u00a0vitro and in a patient-derived xenograft mouse model. These findings suggest that targeting EGR1-mediated metabolic reprogramming to OXPHOS with metformin or IM156 provides a potential therapeutic strategy to overcome ibrutinib resistance in relapsed\/refractory DLBCL or MCL.<\/jats:p>","DOI":"10.1182\/blood.2023020142","type":"journal-article","created":{"date-parts":[[2023,9,22]],"date-time":"2023-09-22T17:05:00Z","timestamp":1695402300000},"page":"1879-1894","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":60,"title":["EGR1-mediated metabolic reprogramming to oxidative phosphorylation contributes to ibrutinib resistance in B-cell lymphoma"],"prefix":"10.1182","volume":"142","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7502-6828","authenticated-orcid":false,"given":"Yunxia","family":"Liu","sequence":"first","affiliation":[{"name":"1Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI"},{"name":"2Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuichi","family":"Kimpara","sequence":"additional","affiliation":[{"name":"1Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI"},{"name":"2Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9179-0188","authenticated-orcid":false,"given":"Nguyet M.","family":"Hoang","sequence":"additional","affiliation":[{"name":"1Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI"},{"name":"2Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6404-7444","authenticated-orcid":false,"given":"Anusara","family":"Daenthanasanmak","sequence":"additional","affiliation":[{"name":"3Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6851-2668","authenticated-orcid":false,"given":"Yangguang","family":"Li","sequence":"additional","affiliation":[{"name":"1Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI"},{"name":"2Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, 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University of Wisconsin School of Medicine and Public Health, Madison, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Longzhen","family":"Song","sequence":"additional","affiliation":[{"name":"2Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI"},{"name":"5Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyue","family":"Gao","sequence":"additional","affiliation":[{"name":"1Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI"},{"name":"2Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samantha","family":"Bebel","sequence":"additional","affiliation":[{"name":"1Department of Medicine, University of Wisconsin School of Medicine and Public Health, 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