Zhao Pin, Malik Samiullah, Xing Shaojun
Guandong Key Laboratory for Biomedical Measurements and Ultrasound Imaging, School of Biomedical Engineering, Shenzhen University Health Science Center, Shenzhen, China.
Department of Pathogen Biology, Shenzhen University Health Science Center, Shenzhen, China.
Front Oncol. 2021 Jul 15;11:677926. doi: 10.3389/fonc.2021.677926. eCollection 2021.
Hepatocellular carcinoma (HCC), is the third leading cause of cancer-related deaths, which is largely caused by virus infection. About 80% of the virus-infected people develop a chronic infection that eventually leads to liver cirrhosis and hepatocellular carcinoma (HCC). With approximately 71 million HCV chronic infected patients worldwide, they still have a high risk of HCC in the near future. However, the mechanisms of carcinogenesis in chronic HCV infection have not been still fully understood, which involve a complex epigenetic regulation and cellular signaling pathways. Here, we summarize 18 specific gene targets and different signaling pathways involved in recent findings. With these epigenetic alterations requiring histone modifications and DNA hyper or hypo-methylation of these specific genes, the dysregulation of gene expression is also associated with different signaling pathways for the HCV life cycle and HCC. These findings provide a novel insight into a correlation between HCV infection and HCC tumorigenesis, as well as potentially preventable approaches. Hepatitis C virus (HCV) infection largely causes hepatocellular carcinoma (HCC) worldwide with 3 to 4 million newly infected cases diagnosed each year. It is urgent to explore its underlying molecular mechanisms for therapeutic treatment and biomarker discovery. However, the mechanisms of carcinogenesis in chronic HCV infection have not been still fully understood, which involve a complex epigenetic regulation and cellular signaling pathways. Here, we summarize 18 specific gene targets and different signaling pathways involved in recent findings. With these epigenetic alterations requiring histone modifications and DNA hyper or hypo-methylation of these specific genes, the dysregulation of gene expression is also associated with different signaling pathways for the HCV life cycle and HCC. These findings provide a novel insight into a correlation between HCV infection and HCC tumorigenesis, as well as potentially preventable approaches.
肝细胞癌（HCC）是癌症相关死亡的第三大主要原因，主要由病毒感染引起。约80%的病毒感染者会发展为慢性感染，最终导致肝硬化和肝细胞癌（HCC）。全球约有7100万丙型肝炎病毒（HCV）慢性感染患者，他们在不久的将来仍有很高的患HCC风险。然而，慢性HCV感染中的致癌机制仍未完全了解，这涉及复杂的表观遗传调控和细胞信号通路。在此，我们总结了近期研究结果中涉及的18个特定基因靶点和不同信号通路。由于这些表观遗传改变需要组蛋白修饰以及这些特定基因的DNA高甲基化或低甲基化，基因表达的失调也与HCV生命周期和HCC的不同信号通路相关。这些发现为HCV感染与HCC肿瘤发生之间的关联以及潜在的可预防方法提供了新的见解。丙型肝炎病毒（HCV）感染在全球范围内是肝细胞癌（HCC）的主要病因，每年有300万至400万新感染病例被诊断出来。探索其潜在分子机制以用于治疗和生物标志物发现迫在眉睫。然而，慢性HCV感染中的致癌机制仍未完全了解，这涉及复杂的表观遗传调控和细胞信号通路。在此，我们总结了近期研究结果中涉及的18个特定基因靶点和不同信号通路。由于这些表观遗传改变需要组蛋白修饰以及这些特定基因的DNA高甲基化或低甲基化，基因表达的失调也与HCV生命周期和HCC的不同信号通路相关。这些发现为HCV感染与HCC肿瘤发生之间的关联以及潜在的可预防方法提供了新的见解。
