{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T06:06:23Z","timestamp":1784700383584,"version":"3.55.0"},"reference-count":150,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T00:00:00Z","timestamp":1784678400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Understanding Human papillomavirus (HPV) oncogenic mechanisms is essential for developing preventive and therapeutic strategies and overcoming therapy resistance in HPV-related cancers. These challenges may arise from the ability of high-risk HPV to subvert host tumor suppressors such as p53 and Rb, and to drive oncogenesis through homologous recombination deficiency (HRD) and multi-network dysregulation. Mechanistically, HPV exerts context-dependent effects on the host DNA damage response (DDR). During episomal replication, E6\/E7 activate DDR and recruit BRCA1\/RAD51 to replication foci to support viral replication without significantly compromising host HR repair. Upon viral integration, however, sustained E6\/E7 expression drives HRD and shifts DNA repair toward error-prone end joining, generating genomic instability that fuels malignant transformation. These alterations are most clearly established in cervical cancer, whereas evidence in HPV-positive non-cervical cancer is more variable and requires further context-specific validation. In parallel, HPV E6\/E7 antagonize transforming growth factor-\u03b2 (TGF-\u03b2)-mediated tumor suppression and, potentially through FAT Atypical Cadherin 4 (FAT4) down-regulation, engage Wnt\/\u03b2-catenin signaling. The resultant elevation of nuclear \u03b2-catenin induces programmed death-ligand 1 (PD-L1) expression promotes immune evasion, stemness, and invasiveness. Of note, while the DDR-TGF-\u03b2-\u03b2-catenin-PD-L1 axis is backed by substantial evidence in HPV-related cancers, certain connections within this pathway are extrapolated from non-HPV models or general pathway biology and are explicitly denoted as such in the main text. With residual p53 activity, HRD may confer initial sensitivity to DNA-damaging agents, but resistance frequently develops\u2014a pattern reminiscent of the initial response followed by acquired resistance observed with immunotherapies in HPV-related cancers. Integrating these mechanistic insights, we propose ablative therapies (e.g., ablation, photodynamic therapy, surgery) for cervical intraepithelial neoplasia (CIN), and for advanced or resistant disease, a synthetic-lethality framework combining genotoxic therapies with DDR inhibitors, targeting DDR-TGF-\u03b2-\u03b2-catenin-PD-L1 axis, and antiviral approaches. The proposed therapeutic strategies, however, should be interpreted with caution, as their evidence base varies across tumor types and warrants further investigation.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1907171","type":"journal-article","created":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T05:52:22Z","timestamp":1784699542000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Rewired DDR-TGF-\u03b2-\u03b2-catenin-PD-L1 axis accelerates progression and shapes therapy in human papillomavirus-driven cancer"],"prefix":"10.3389","volume":"17","author":[{"given":"Wei","family":"Liu","sequence":"first","affiliation":[{"name":"Hunan Cancer Hospital, Affiliated Hospital of Xiangya Medical School, Central South University","place":["Changsha, Hunan, China"]},{"name":"Shaoyang Central Hospital","place":["Shaoyang, Hunan, China"]},{"name":"Key Laboratory of Carcinogenesis of Ministry of Health, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shanmei","family":"Chen","sequence":"additional","affiliation":[{"name":"Hunan Cancer Hospital, Affiliated Hospital of Xiangya Medical School, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liwei","family":"Wang","sequence":"additional","affiliation":[{"name":"Hunan Cancer Hospital, Affiliated Hospital of Xiangya Medical School, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Xiang","sequence":"additional","affiliation":[{"name":"Hunan Cancer Hospital, Affiliated Hospital of Xiangya Medical School, Central South University","place":["Changsha, Hunan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siyi","family":"Tao","sequence":"additional","affiliation":[{"name":"Second Xiangya 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