{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T21:08:50Z","timestamp":1791493730562,"version":"4.3.4"},"reference-count":101,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2022,5,18]],"date-time":"2022-05-18T00:00:00Z","timestamp":1652832000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"University of Texas at Dallas (Delk)","award":["NSF1202008"],"award-info":[{"award-number":["NSF1202008"]}]},{"name":"Louis Stocks Alliance for Minority Student Participation","award":["NSF1202008"],"award-info":[{"award-number":["NSF1202008"]}]},{"DOI":"10.13039\/100000001","name":"National Science Foundation","doi-asserted-by":"publisher","award":["NSF1202008"],"award-info":[{"award-number":["NSF1202008"]}],"id":[{"id":"10.13039\/100000001","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>While meant for wound healing and immunity in response to injury and infection, inflammatory signaling is usurped by cancerous tumors to promote disease progression, including treatment resistance. The interleukin-1 (IL-1) inflammatory cytokine family functions in wound healing and innate and adaptive immunity. Two major, closely related IL-1 family members, IL-1\u03b1 and IL-1\u03b2, promote tumorigenic phenotypes and contribute to treatment resistance in cancer. IL-1 signaling converges on transactivation of the Nuclear Factor Kappa B (NF-\u03baB) and Activator protein 1 (AP-1) transcription factors. NF-\u03baB and AP-1 signaling are also activated by the inflammatory cytokine Tumor Necrosis Factor Alpha (TNF\u03b1) and microbe-sensing Toll-Like Receptors (TLRs). As reviewed elsewhere, IL-1, TNF\u03b1, and TLR can promote cancer progression through NF-\u03baB or AP-1. In this review, we focus on what is known about the role of IL-1\u03b1 and IL-1\u03b2 in breast cancer (BCa) progression and therapeutic resistance, and state evidence for the role of NF-\u03baB in mediating IL-1-induced BCa progression and therapeutic resistance. We will present evidence that IL-1 promotes BCa cell proliferation, BCa stem cell expansion, angiogenesis, and metastasis. IL-1 also regulates intracellular signaling and BCa cell hormone receptor expression in a manner that confers a growth advantage to the tumor cells and allows BCa cells to evade therapy. As such, the IL-1 receptor antagonist, anakinra, is in clinical trials to treat BCa and multiple other cancer types. This article presents a review of the literature from the 1990s to the present, outlining the evidence supporting a role for IL-1 and IL-1-NF-\u03baB signaling in BCa progression.<\/jats:p>","DOI":"10.3390\/cells11101673","type":"journal-article","created":{"date-parts":[[2022,5,18]],"date-time":"2022-05-18T11:59:37Z","timestamp":1652875177000},"page":"1673","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":61,"title":["Interleukin-1 and Nuclear Factor Kappa B Signaling Promote Breast Cancer Progression and Treatment Resistance"],"prefix":"10.3390","volume":"11","author":[{"given":"Sydney","family":"Diep","sequence":"first","affiliation":[{"name":"Biological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahita","family":"Maddukuri","sequence":"additional","affiliation":[{"name":"Biological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie","family":"Yamauchi","sequence":"additional","affiliation":[{"name":"Biological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ganamee","family":"Geshow","sequence":"additional","affiliation":[{"name":"Biological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9482-3830","authenticated-orcid":false,"given":"Nikki A.","family":"Delk","sequence":"additional","affiliation":[{"name":"Biological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,5,18]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1003","DOI":"10.1016\/j.immuni.2013.11.010","article-title":"The Interleukin-1 Family: Back to the Future","volume":"39","author":"Garlanda","year":"2013","journal-title":"Immunity"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"2964","DOI":"10.1007\/s00018-008-8064-8","article-title":"TLR-4, IL-1R and TNF-R signaling to NF-kappaB: Variations on a common theme","volume":"65","author":"Verstrepen","year":"2008","journal-title":"Cell. 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