乙型肝炎病毒感染及其导致的持续性炎症是肝硬化和肝细胞癌的重要原因。乙肝病毒感染和炎症均可以通过调控microRNA表达影响致癌过程。表达异常的microRNA在慢性炎症恶性转化过程中起重要调控作用。部分microRNA通过促进乙型肝炎病毒的复制或炎症反应因子的表达加剧炎症反应;或通过激活肝星形细胞或产生胶原蛋白来加速纤维化过程;还可以通过打破促癌因子与抑癌因子的平衡来促进癌症的发生与发展。促炎介质可以通过调控microRNA表达等表观遗传机制,进而促进HBV诱导肝细胞癌的进化发育过程。本文初步探讨了持续性炎症导致microRNA表达异常的过程中可能存在的机制和异常表达的microRNA在慢性乙型肝炎、肝硬化、肝细胞癌中的作用。
Hepatitis B virus (HBV) infection and the subsequent persistent inflammation are the important factors that facilitate the development of liver cirrhosis and hepatocellular carcinoma. Both HBV infection and persistent inflammation can affect carcinogenesis via regulating microRNA expression. Aberrant expression of microRNAs plays an important role in regulating the malignant transformation of chronic inflammation. Some microRNAs can aggravate inflammation via increasing HBV replication or expression of inflammatory factors, some can promote fibrosis process via activating hepatic stellate cells or producing collagen proteins, and some can promote cancer progression by affecting the balance between cancer promoting factors and tumor suppressor factors. Proinflammatory molecules can promote Evo-Dev of HBV-induced hepatocellular carcinoma through epigenetic regulation including regulating the expression of microRNAs. Here in this review we discussed the potential mechanisms by which persistent inflammation induces aberrant expression of microRNAs and the role of dysregulated microRNAs in the development of chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma.