丙型肝炎病毒 (HCV) 长期感染全世界约 1.7 亿人，是肝细胞癌 (HCC) 的已知病原体。 HCV 介导的致癌作用的分子机制尚不完全清楚。这篇综述文章重点关注 NS3 的致癌潜力，NS3 是一种对细胞具有转化作用的病毒蛋白，尽管其确切机制仍难以捉摸。与更广泛研究的 Core 和 NS5A 蛋白不同，NS3 在癌症发展中的作用不太明确，但很关键。研究表明，NS3 与多种致癌过程有关，例如增殖信号传导、细胞死亡抵抗、基因组不稳定和突变、侵袭和转移、肿瘤相关炎症、免疫逃避和复制永生。了解 NS3 等病毒蛋白对细胞转化的直接影响对于阐明 HCV 在 HCC 发展中的作用至关重要。总体而言，这篇综述阐明了 NS3 促进肝癌发生的分子机制，并强调了其在 HCV 相关 HCC 背景下的重要性，强调需要进一步研究其特定的分子和细胞作用。© 2024。作者（s）。

Hepatitis C virus (HCV) chronically infects approximately 170 million people worldwide and is a known etiological agent of hepatocellular carcinoma (HCC). The molecular mechanisms of HCV-mediated carcinogenesis are not fully understood. This review article focuses on the oncogenic potential of NS3, a viral protein with transformative effects on cells, although the precise mechanisms remain elusive. Unlike the more extensively studied Core and NS5A proteins, NS3's roles in cancer development are less defined but critical. Research indicates that NS3 is implicated in several carcinogenic processes such as proliferative signaling, cell death resistance, genomic instability and mutations, invasion and metastasis, tumor-related inflammation, immune evasion, and replicative immortality. Understanding the direct impact of viral proteins such as NS3 on cellular transformation is crucial for elucidating HCV's role in HCC development. Overall, this review sheds light on the molecular mechanisms used by NS3 to contribute to hepatocarcinogenesis, and highlights its significance in the context of HCV-associated HCC, underscoring the need for further investigation into its specific molecular and cellular actions.© 2024. The Author(s).