The crucial role of high mobility group AT-hook 1 (HMGA1) proteins in nuclear processes such as gene transcription, DNA replication, and chromatin remodeling is undeniable. Elevated levels of HMGA1 have been associated with unfavorable clinical outcomes and adverse differentiation status across various cancer types. HMGA1 regulates a diverse array of biological pathways, including tumor necrosis factor-alpha/nuclear factor-kappa B (TNF‐α/NF‐κB), epidermal growth factor receptor (EGFR), Hippo, Rat sarcoma/extracellular signal-regulated kinase (Ras/ERK), protein kinase B (Akt), wingless-related integration site/beta-catenin (Wnt/beta‐catenin), and phosphoinositide 3-kinase/protein kinase B (PI3‐K/Akt). While researchers have extensively investigated tumors in the reproductive, digestive, urinary, and hematopoietic systems, mounting evidence suggests that HMGA1 plays a critical role as a tumorigenic factor in tumors across all functional systems. Given its broad interaction network, HMGA1 is an attractive target for viral manipulation. Some viruses, including herpes simplex virus type 1, human herpesvirus 8, human papillomavirus, JC virus, hepatitis B virus, human immunodeficiency virus type 1, severe acute respiratory syndrome Coronavirus 2, and influenza viruses, utilize HMGA1 influence for infection. This interaction, particularly in oncogenesis, is crucial. Apart from the direct oncogenic effect of some of the mentioned viruses, the hit-and-run theory postulates that viruses can instigate cancer even before being completely eradicated from the host cell, implying a potentially greater impact of viruses on cancer development than previously assumed. This review explores the interplay between HMGA1, viruses, and host cellular machinery, aiming to contribute to a deeper understanding of viral-induced oncogenesis, paving the way for innovative strategies in cancer research and treatment.

高迁移率基团 AT-hook 1 (HMGA1) 蛋白在基因转录、DNA 复制和染色质重塑等核过程中的关键作用是不可否认的。HMGA1 水平升高与各种癌症类型的不良临床结果和不良分化状态相关。HMGA1 调节多种生物学途径，包括肿瘤坏死因子-α/核因子-κ B (TNF-α/NF-κB)、表皮生长因子受体 (EGFR)、Hippo、大鼠肉瘤/细胞外信号调节激酶 ( Ras/ERK)、蛋白激酶 B (Akt)、无翼相关整合位点/β-连环蛋白 (Wnt/β-连环蛋白) 和磷酸肌醇 3-激酶/蛋白激酶 B (PI3-K/Akt)。虽然研究人员广泛研究了生殖、消化、泌尿和造血系统中的肿瘤，但越来越多的证据表明，HMGA1 作为所有功能系统肿瘤的致瘤因子发挥着关键作用。鉴于其广泛的相互作用网络，HMGA1 是病毒操作的一个有吸引力的目标。一些病毒，包括单纯疱疹病毒1型、人疱疹病毒8、人乳头瘤病毒、JC病毒、乙型肝炎病毒、人类免疫缺陷病毒1型、严重急性呼吸综合征冠状病毒2和流感病毒，利用HMGA1影响进行感染。这种相互作用，特别是在肿瘤发生中，至关重要。除了上述一些病毒的直接致癌作用外，肇事逃逸理论还假设，病毒甚至在从宿主细胞中完全根除之前就可以引发癌症，这意味着病毒对癌症发展的影响可能比之前的假设更大。本综述探讨了 HMGA1、病毒和宿主细胞机制之间的相互作用，旨在有助于更深入地了解病毒诱导的肿瘤发生，为癌症研究和治疗的创新策略铺平道路。