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Moreover, radiotherapy-resistant TNBC (RT-R-TNBC) exhibits enhanced chemotherapy resistance and invasiveness. Therefore, there is a critical need for innovative treatments for RT-R-TNBC and TNBC patients. Our previous study indicated that NK cells exhibit reduced cytotoxicity against RT-R-TNBCs due to human leukocyte antigen class I histocompatibility antigen, alpha chain E (HLA-E) upregulation. Thus, this study aimed to identify the mechanism responsible for the upregulation of HLA-E and suggest potential therapeutic targets for overcoming the RT-resistance of TNBC. We found that HLA-E expression was significantly higher in TNBC tumor tissues than in normal epithelial tissues and non-TNBC tissues, correlating with A2AR levels. In addition, MDA-MB-231 (TNBC) and RT-R-MDA-MB-231 (RT-R-TNBC) showed an A2AR-dependent HLA-E overexpression. NK cell-mediated cytotoxicity against MDA-MB-231 and RT-R-MDA-MB-231 was reduced and restored by A2AR or STAT1 knockdown. Interestingly, STAT1 phosphorylation (Y701) by adenosine (ADO) aligned with the HLA-E expression pattern by ADO, and fludarabine, a STAT1 inhibitor, effectively reduced phospho-STAT1 (Y701) levels but not phospho-STAT1 (S727) levels. Fludarabine also inhibited ADO-induced HLA-E expression in MDA-MB-231 and RT-R-MDA-MB-231, including basal HLA-E expression in RT-R-MDA-MB-231. Additionally, fludarabine reduced tumor progression, lung metastasis, HLA-E expression, and phospho-STAT1 (Y701) in RT-R-MDA-MB-231-injected mice. Moreover, monalizumab, an NKG2A monoclonal antibody, significantly reduced tumor progression and lung metastasis with increased population of cytotoxic NK cells (CD25 + NK1.1+ and CD69 + NK1.1+) in the inguinal lymph nodes of RT-R-MDA-MB-231-injected mice. This study suggests that the A2AR-phospho-STAT1 (Y701)-HLA-E axis may serve as an alternative target for overcoming RT-resistance in TNBC.<\/jats:p>","DOI":"10.1093\/carcin\/bgaf069","type":"journal-article","created":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T11:29:58Z","timestamp":1760959798000},"source":"Crossref","is-referenced-by-count":2,"title":["A2AR-phospho-STAT1 (Y701)-HLA-E axis as a potential immune modulatory pathway in radiotherapy-resistant triple negative breast cancer"],"prefix":"10.1093","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-0058-8229","authenticated-orcid":false,"given":"Young Shin","family":"Ko","sequence":"first","affiliation":[{"name":"Department of Pharmacology, College of Medicine, Institute of Medical Sciences, Gyeongsang National University , Jinjudaero 816 Bungil 15, Jinju 52727 ,","place":["Republic of Korea"]},{"name":"Department of Convergence Medical Science, Gyeongsang National University , Jinjudaero 816 Bungil 15, 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Gyeongsang National University , Jinjudaero 816 Bungil 15, Jinju 52727 ,","place":["Republic of Korea"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9159-7575","authenticated-orcid":false,"given":"Jong Sil","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pathology, College of Medicine, Institute of Medical Sciences, Gyeongsang National University , Jinjudaero 816 Bungil 15, Jinju 52727 ,","place":["Republic of Korea"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9484-7792","authenticated-orcid":false,"given":"Dong Chul","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Pathology, College of Medicine, Institute of Medical Sciences, Gyeongsang National University , Jinjudaero 816 Bungil 15, Jinju 52727 ,","place":["Republic of 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