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Adv."],"published-print":{"date-parts":[[2026,9,25]]},"abstract":"<jats:p>\n                    The RNF43 p.G659fs (\n                    <jats:italic toggle=\"yes\">\n                      RNF43\n                      <jats:sup>659mut<\/jats:sup>\n                    <\/jats:italic>\n                    ) mutation occurs in 8% of colorectal cancers (CRCs) and is enriched in microsatellite instability\u2013high (MSI-H) tumors. Although\n                    <jats:italic toggle=\"yes\">\n                      RNF43\n                      <jats:sup>659mut<\/jats:sup>\n                    <\/jats:italic>\n                    promotes tumor growth through phosphatidylinositol 3-kinase\/protein kinase B\/mechanistic target of rapamycin (PI3K\/AKT\/mTOR) activation independent of WNT signaling, its immunologic effects are poorly defined. We show that\n                    <jats:italic toggle=\"yes\">\n                      RNF43\n                      <jats:sup>659mut<\/jats:sup>\n                    <\/jats:italic>\n                    shapes an immunosuppressive natural killer (NK) cell landscape in MSI-H CRC. Single-cell RNA sequencing and multiplex immunohistochemistry revealed increased NK cell infiltration in\n                    <jats:italic toggle=\"yes\">\n                      RNF43\n                      <jats:sup>659mut<\/jats:sup>\n                    <\/jats:italic>\n                    tumors, yet these cells displayed inhibitory phenotypes. Bulk RNA sequencing and flow cytometry of NK cells cocultured with\n                    <jats:italic toggle=\"yes\">\n                      RNF43\n                      <jats:sup>659mut<\/jats:sup>\n                    <\/jats:italic>\n                    isogenic lines and MSI-H patient-derived organoids demonstrated reduced functional NK subsets, decreased activation markers, increased inhibitory receptors, and impaired cytotoxicity. Mechanistically,\n                    <jats:italic toggle=\"yes\">\n                      RNF43\n                      <jats:sup>659mut<\/jats:sup>\n                    <\/jats:italic>\n                    -mediated PI3K\/AKT activation induced HLA-E expression, suppressing NK cell function. Pharmacological or small interfering RNA\u2013mediated PI3K\/AKT inhibition restored NK cell activity and enhanced tumor cell killing. Spatial analysis of MSI-H patient tumors revealed close proximity between NKG2A\n                    <jats:sup>+<\/jats:sup>\n                    NK cells and HLA-E\n                    <jats:sup>+<\/jats:sup>\n                    tumor cells, which were themselves adjacent to PI3K\/AKT-activated tumor cells, highlighting a localized immunosuppressive niche. These findings uncover an immune evasion mechanism in MSI-H CRC, implicating the PI3K\/AKT-HLA-E\/NKG2A axis as a promising therapeutic target to overcome immunotherapy resistance.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.adz6907","type":"journal-article","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T17:59:49Z","timestamp":1790186389000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K\/AKT\/mTOR signaling and HLA-E up-regulation"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0747-5637","authenticated-orcid":true,"given":"Pushpamali","family":"De Silva","sequence":"first","affiliation":[{"name":"Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA."},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7676-0645","authenticated-orcid":true,"given":"Samantha","family":"Fitzgerald","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA."},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-1992-3197","authenticated-orcid":true,"given":"Jules","family":"Cazaubiel","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA."},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5016-0112","authenticated-orcid":true,"given":"Kristin","family":"Qian","sequence":"additional","affiliation":[{"name":"Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8368-0299","authenticated-orcid":true,"given":"Matan","family":"Hofree","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA."},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4702-7705","authenticated-orcid":true,"given":"Jia-Ren","family":"Lin","sequence":"additional","affiliation":[{"name":"Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roxanne","family":"Pelletier","sequence":"additional","affiliation":[{"name":"Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4599-7719","authenticated-orcid":true,"given":"Mariana","family":"Lopez Leon","sequence":"additional","affiliation":[{"name":"Laboratory of Systems Pharmacology, Harvard Medical School, Boston, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-9693-6730","authenticated-orcid":true,"given":"Phuong Vu Mai","family":"Ho","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA."},{"name":"Broad Institute of MIT and Harvard, Cambridge, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasutoshi","family":"Takashima","sequence":"additional","affiliation":[{"name":"Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8683-2996","authenticated-orcid":true,"given":"Juha P","family":"V\u00e4yrynen","sequence":"additional","affiliation":[{"name":"Translational Medicine Research Unit, Medical Research Center Oulu, Oulu University Hospital, and University of Oulu, Oulu, Finland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-5125-1129","authenticated-orcid":true,"given":"Kosuke","family":"Matsuda","sequence":"additional","affiliation":[{"name":"Department of Pathology, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, MA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0182-5269","authenticated-orcid":true,"given":"Tomotaka","family":"Ugai","sequence":"additional","affiliation":[{"name":"Department of Pathology, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, MA, USA."},{"name":"Department of Epidemiology, Harvard T.H. 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