{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T06:54:37Z","timestamp":1788245677959,"version":"build-2803163510"},"reference-count":101,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,1,10]],"date-time":"2025-01-10T00:00:00Z","timestamp":1736467200000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Medicine"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Glioblastoma (GBM) is the most common primary brain tumor in adults and has a median survival of less than 15 months. Advancements in the field of epigenetics have expanded our understanding of cancer biology and helped explain the molecular heterogeneity of these tumors. B\u2010cell\u2010specific Moloney murine leukemia virus insertion site\u20101 (Bmi\u20101) is a member of the highly conserved polycomb group (PcG) protein family that acts as a transcriptional repressor of multiple genes, including those that determine cell proliferation and differentiation. We hereby aim to explore the specific involvement of Bmi\u20101 in glioma pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A comprehensive narrative review was employed using \u201cPubMed\u201d. Articles were screened for relevance specific keywords and medical subject headings (MeSH) terms related to the topic combined with Boolean operators (AND, OR). Keywords and MeSH terms included the following: \u201cglioma\u201d, \u201cpolycomb repressive complex 1\u201d, and \u201cBmi1\u201d.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In GBMs, several reports have shown that Bmi\u20101 is overexpressed and might serve as a prognostic biomarker. We\u2009find\u2009that\u2009Bmi\u20101 participates in regulating the gene expression and chromatin structure of several tumor suppressor genes or cell cycle inhibitors. Bmi\u20101 has a critical role in modulating the tumor microenvironment to support the plasticity of GBM stem cells.We explore Bmi\u20101's involvement in maintaining glioma stem cell (GSC) proliferation and senescence evasion upon regulating the chromatin structure of several tumor suppressor genes, cell cycle inhibitors, or stem cell genes in tumor cells. Additionally, we analyze Bmi\u20101's involvement in modulating the DNA repair machinery or activating anti\u2010apoptotic pathways to confer therapy resistance. Importantly, our research discusses the importance of targeting Bmi\u20101 that could be a promising therapeutic target for GBM treatment. Bmi\u20101 activates and interacts with NF\u2010\u03baB to promote angiogenesis and invasion, regulates the INK4a\u2010ARF locus, and interacts with various microRNAs to influence tumor progression and proliferation.\u2009In addition, Bmi\u20101 confers radioresistance and chemotherapy by promoting cell senescence evasion and DNA repair.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Bmi\u20101 regulates self\u2010renewal, proliferation, and differentiation of GBM cells, promoting stemness and therapy resistance. Targeting Bmi\u20101 could be a promising novel therapeutic strategy for\u2009GBM\u2009treatment.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cam4.70566","type":"journal-article","created":{"date-parts":[[2025,1,10]],"date-time":"2025-01-10T07:45:30Z","timestamp":1736495130000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Insights Into the Role of Bmi\u20101 Deregulation in Promoting Stemness and Therapy Resistance in Glioblastoma: A Narrative Review"],"prefix":"10.1002","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-5886-148X","authenticated-orcid":false,"given":"Fatima","family":"Shaalan","sequence":"first","affiliation":[{"name":"Faculty of Medical Sciences, Neuroscience Research Center Lebanese University  Hadath 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