{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:18:56Z","timestamp":1791994736192,"version":"4.4.0"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T00:00:00Z","timestamp":1769472000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82573312 to Q.Z"],"award-info":[{"award-number":["82573312 to Q.Z"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82525047 to X.W"],"award-info":[{"award-number":["82525047 to X.W"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82403659 to C.L"],"award-info":[{"award-number":["82403659 to C.L"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Clinical Research Foundation for the Prevention and Treatment of Collaborative Innovation Center for Cancer Personalized Medicine of Nanjing Medical University","award":["2024CICCPMHR036 to Q.Z"],"award-info":[{"award-number":["2024CICCPMHR036 to Q.Z"]}]},{"name":"Clinical Research Foundation for the Prevention and Treatment of Collaborative Innovation Center for Cancer Personalized Medicine of Nanjing Medical University","award":["2024CICCPMHR015 to X.W"],"award-info":[{"award-number":["2024CICCPMHR015 to X.W"]}]},{"name":"Jiangsu Province High-Level Hospital Pairing Assistance Construction Funds","award":["zdlyg05&gt; to K.Y"],"award-info":[{"award-number":["zdlyg05&gt; to K.Y"]}]},{"name":"Research Personnel Cultivation Programme of Zhongda Hospital Southeast University","award":["CZXM-GSP-RC-152 to K.Y"],"award-info":[{"award-number":["CZXM-GSP-RC-152 to K.Y"]}]},{"name":"Medical Science and Technology Development Foundation of Nanjing","award":["ZKX22041 to K.Y"],"award-info":[{"award-number":["ZKX22041 to K.Y"]}]},{"DOI":"10.13039\/501100004608","name":"Natural Science Foundation of Jiangsu Province","doi-asserted-by":"publisher","award":["BK20241130 to C.L"],"award-info":[{"award-number":["BK20241130 to C.L"]}],"id":[{"id":"10.13039\/501100004608","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Glioblastoma (GBM) is a highly aggressive brain tumor, with glioblastoma stem cells (GSCs) occupying the pinnacle of a complex tumor microenvironment (TME), conferring therapeutic resistance. The TME plays a role in tumor development by creating a niche rich in reactive oxygen species (ROS) through oxidative stress (OS). Here, we identified NAD(P)H: quinone oxidoreductase 1 (NQO1) as an essential regulatory factor in antioxidant stress response, which is key to maintaining GSCs and the immunosuppressive TME.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Proteomics analysis and epigenetic profiling using H3K27ac ChIP-sequencing and single-cell RNA sequencing were performed to define the high enrichment of NQO1 in GBM. In vitro and in vivo loss-of-function genetic and pharmacologic assays were conducted to evaluate the effect of NQO1 in GSC proliferation and self-renewal. Patient-derived GSCs and xenograft murine models were using to investigate the tumor-intrinsic and extrinsic mechanisms to confers resistance to OS and reprogram the immunosuppressive TME.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>NQO1 was preferentially expressed in GSCs and regulated ROS levels, preserving the stability of nuclear Lamin B1 and inhibiting cGAS-type I interferon signaling, which helps to remodel the immunosuppressive TME. Furthermore, nuclear factor erythroid 2-related factor 2 (NRF2) transcriptionally regulates NQO1, suppressing type I interferon signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>NQO1 plays critical roles at both the cell-autonomous and cell-extrinsic levels for clinical treatment. Targeting NQO1 and its downstream signaling pathways, including \u03b2-lapachone and immune checkpoint inhibitors such as anti-PD-1 therapy, enhances our understanding of the interactions between GSCs, OS, and the TME. This offers promising new avenues for clinical intervention in GBM.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/neuonc\/noag015","type":"journal-article","created":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T12:59:49Z","timestamp":1769086789000},"page":"1117-1132","source":"Crossref","is-referenced-by-count":4,"title":["NAD(P)H: quinone oxidoreductase 1-mediated oxidative stress resistance and tumor microenvironment remodeling in glioblastoma"],"prefix":"10.1093","volume":"28","author":[{"given":"Yangqing","family":"Li","sequence":"first","affiliation":[{"name":"Ministry of Education Key Laboratory of Model Animals for \u00adDisease Study, Model Animal Research Center, Medical School of Nanjing University, National Resource Center for Mutant Mice , Nanjing, Jiangsu,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Kang","sequence":"additional","affiliation":[{"name":"National Health Commission Key Laboratory of 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