原发性肝细胞癌（hepatocellular carcinoma，HCC）是最常见的癌症之一，是全球第二大癌症相关死亡原因。已开发了许多治疗方案以治愈该疾病，但预期寿命仍然较低。因此，迫切需要探索新的选择性、特异性和稳健的诊断标志物，以便有效早期识别该疾病。除了诊断外，预后标志物还可以确定治疗的有效性，而miRNA是HCC诊断和预后的优秀工具。此外，少数miRNA的改变表达谱促进了HCC细胞的迁移和侵袭，选择性上调或下调这些相关基因可能有助于减轻该疾病。一方面，已发现少数miRNA可以增进血管生成，这是肿瘤生长的重要步骤；另一方面，特定miRNA的上调被报道可抑制HCC细胞的血管生成和肿瘤生长。胞外小RNA在促进血管生成、增加内皮细胞通透性、管腔形成以及向肝肺组织转移方面具有显著意义。miRNA还与化疗耐药性和自噬的抑制有关。在HCC组织中鉴定新的miRNA并确定其差异表达可能成为诊断、预后和治疗的潜在工具，以增强HCC患者的预期寿命和生活质量。本综述总结了与HCC相关研究的最新进展。© 2023 John Wiley & Sons A/S.

Hepatocellular carcinoma (HCC) is one of the most common cancers and is responsible for the second cancer-related death globally. Many treatment regimens have been developed to cure the disease; however, life expectancy is still low. Therefore, there is an urgent need to explore new selective, specific, and robust diagnosis markers for efficient early recognition of the ailment. Along with the diagnosis, the treatment's effectiveness can be determined by prognostic markers, and miRNAs are excellent tools for the diagnosis and prognosis of HCC. In addition, the altered expression profile of a few miRNAs promotes HCC cell migration and invasion, and selective up- or downregulation of these responsible genes may help mitigate the disorder. On one hand, few of the miRNAs have been found to enhance angiogenesis, a crucial step of tumor growth; on the other hand, upregulation of specific miRNAs is reported to suppress angiogenesis and resulting tumor growth of HCC cells. Exosomal miRNAs have significant implications in promoting angiogenesis, increased endothelial cell permeability, tube formation, and metastasis to hepatic and pulmonary tissues. miRNA also attributes to drug resistance toward chemotherapy and the prevention of autophagy also. Identifying novel miRNA and determining their differential expression in HCC tissue may serve as a potential tool for diagnosis, prognosis, and therapy to enhance the life expectancy and quality of life of HCC patients. In the present review, we have summarized the recent advances in HCC-related research.© 2023 John Wiley & Sons A/S.