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This review comprehensively examines how oncoviruses\u2014including Epstein\u2010Barr virus (EBV), Kaposi's sarcoma herpesvirus (KSHV), hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomavirus (HPV), and others\u2014remodel key cytoskeletal components such as actin microfilaments, intermediate filaments (IFs), and microtubules (MTs). These virus\u2010induced alterations facilitate epithelial\u2010mesenchymal transition (EMT), enhance cell migration, and enable extracellular matrix degradation, thereby fostering tumor spread. We discuss specific mechanisms, including viral protein interactions and the deregulation of signaling pathways such as Rho GTPases and mTOR, which collectively orchestrate cytoskeletal dynamics to support invasion and metastasis. Furthermore, this review highlights emerging therapeutic opportunities, including targeting FSCN1 (Fascin Actin\u2010bundling Protein 1, FSCN1) inhibition or using small\u2010molecule inhibitors to disrupt oncovirus\u2010mediated cytoskeletal changes and impede tumor progression. By bridging virology and cancer biology, this review provides novel insights for developing precision antimetastatic strategies and underscores the pivotal role of viral\u2010cytoskeletal interplay in oncology.<\/jats:p>","DOI":"10.1002\/cbf.70144","type":"journal-article","created":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T05:36:17Z","timestamp":1764221777000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Cytoskeletal Remodeling by Oncoviruses: A Key Factor in Tumor Invasion and Metastasisa"],"prefix":"10.1002","volume":"43","author":[{"given":"Yue","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Pathogenic Biology, School of Basic Medicine Qingdao University Qingdao China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pathogenic Biology, School of Basic Medicine Qingdao 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