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Transl. Med."],"published-print":{"date-parts":[[2026,7,8]]},"abstract":"<jats:p>\n                    Glioblastoma (GBM) is a devastating cancer with a dismal prognosis. Current treatment includes temozolomide (TMZ), which is more effective in about 50% of GBMs that have O\n                    <jats:sup>6<\/jats:sup>\n                    -\n                    <jats:italic toggle=\"yes\">methylguanine DNA methyltransferase<\/jats:italic>\n                    (\n                    <jats:italic toggle=\"yes\">MGMT<\/jats:italic>\n                    ) promoter methylation. MGMT is a DNA repair protein that reverses TMZ-induced DNA damage. EGFR is a prime oncogene in GBM. Here, we report that EGFR inhibition induced the down-regulation of MGMT in GBM cells, revealing a previously unidentified link between EGFR signaling and response to TMZ. EGFR inhibition led to activation of two transcription factors, activator protein-1 (AP-1), which repressed MGMT transcription, and nuclear factor \u03baB (NF-\u03baB), which up-regulated\n                    <jats:italic toggle=\"yes\">MGMT<\/jats:italic>\n                    transcription. EGFR inhibition also induced AP-1\u2013mediated transcription of miR-616. miR-616 inhibited both MGMT translation and NF-\u03baB activation. Thus, the overall effect of EGFR inhibition was down-regulation of MGMT expression. In addition, we provided an explanation for the prior failure of clinical trials that used concomitant EGFR tyrosine kinase inhibitors (TKIs) and TMZ. TMZ up-regulated MGMT, and concomitant treatment with EGFR TKIs and TMZ failed to down-regulate MGMT. However, pretreatment with EGFR TKIs followed by TMZ efficiently down-regulated MGMT and enhanced TMZ sensitivity in experimental models. Posttreatment tumor tissues from two clinical trials were used to validate these findings. We demonstrated that EGFR inhibitors induced down-regulation of MGMT in posttreatment resected tumor tissues from patients with GBM and the failure of EGFR inhibition to down-regulate MGMT if TMZ was used concomitantly. These data support using EGFR TKIs before TMZ treatment as a therapeutic approach in\n                    <jats:italic toggle=\"yes\">MGMT<\/jats:italic>\n                    unmethylated GBM.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adx8398","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T17:58:12Z","timestamp":1783533492000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":3,"title":["EGFR inhibition down-regulates MGMT and enhances responsiveness to temozolomide in glioblastoma"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-4032-5199","authenticated-orcid":true,"given":"Arifa","family":"Nayab","sequence":"first","affiliation":[{"name":"Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3298-3959","authenticated-orcid":true,"given":"Nouman","family":"Mughal","sequence":"additional","affiliation":[{"name":"Department of Surgery, Section of Neurosurgery, Department of Surgery, Aga Khan University Hospital, Karachi 74800, Pakistan."},{"name":"Department of Biological and Biomedical Sciences, Aga Khan University Hospital, Karachi 74800, Pakistan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4490-4453","authenticated-orcid":true,"given":"Meher","family":"Angez","sequence":"additional","affiliation":[{"name":"Department of Surgery, Section of Neurosurgery, Department of Surgery, Aga Khan University Hospital, Karachi 74800, Pakistan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sansi","family":"Xing","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Texas Southwestern 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