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The overexpression of EGFR has been linked to its potential role in modulating major histocompatibility complex class I (MHC-I) molecules. We discovered that EGFR, operating in a kinase-independent manner, played a role in stabilizing the expression of SLC7A11, which subsequently inhibited MHC-I antigen presentation. This mechanism, in turn, provided protection to NPC cells against T cell-mediated cytotoxicity. The underlying molecular processes revealed that the high and stable expression of SLC7A11 hindered the nuclear entry of GR, thereby suppressing TAP1 transcription and the presentation of MHC-I molecules. Additionally, elevated SLC7A11 expression led to an increase in FAF2 expression and triggered ERAD-dependent degradation of MHC-I, resulting in a reduction of MHC-I molecules on the cell membrane. The NPC patients exhibiting high EGFR and low MHC-I expression, combined with a scarcity of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells (EGFR\n                    <jats:sup>high<\/jats:sup>\n                    MHC-I\n                    <jats:sup>low<\/jats:sup>\n                    CD8\n                    <jats:sup>few<\/jats:sup>\n                    phenotype), experienced considerably shorter overall survival times compared to other situations. What is more, our study demonstrated that sorafenib had the capability to enhance the MHC-I antigen presentation process, thereby facilitating T cell-mediated killing of NPC cells via targeting SLC7A11. Consequently, targeting SLC7A11 with sorafenib emerges as a promising therapeutic strategy for the treatment of NPC.\n                  <\/jats:p>","DOI":"10.1038\/s41419-024-07327-9","type":"journal-article","created":{"date-parts":[[2025,1,16]],"date-time":"2025-01-16T09:46:44Z","timestamp":1737020804000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Targeting EGFR-binding protein SLC7A11 enhancing antitumor immunity of T cells via inducing MHC-I antigen presentation in nasopharyngeal carcinoma"],"prefix":"10.1038","volume":"16","author":[{"given":"Haihua","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1486-9909","authenticated-orcid":false,"given":"Songqing","family":"Fan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuting","family":"Zhan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao","family":"Du","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiadi","family":"Luo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongjing","family":"Zang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9567-9295","authenticated-orcid":false,"given":"Shuping","family":"Peng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2336-3301","authenticated-orcid":false,"given":"Weiyuan","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,1,16]]},"reference":[{"key":"7327_CR1","doi-asserted-by":"publisher","first-page":"64","DOI":"10.1016\/S0140-6736(19)30956-0","volume":"394","author":"Y-P Chen","year":"2019","unstructured":"Chen Y-P, Chan AT, Le Q-T, Blanchard P, Sun Y, Ma J. 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