作为自噬机制的关键组分，自噬相关基因5（ATG5）对于自噬体形成至关重要。自噬参与了各种恶性肿瘤的转化和进展，但ATG5在肝细胞癌（HCC）中的作用尚待阐明。本研究评估了89对肝肿瘤和癌旁正常组织中ATG5的表达情况，并评估了ATG5表达与临床病理特征或预后的相关性。此外，还分别对年轻患者组和老年患者组进行了临床特殊分析，并探讨了评估总生存和无病生存的示意图。我们的研究表明，在肿瘤标本中，ATG5水平高于癌旁正常组织。升高的ATG5水平与血清α-胎蛋白（AFP）呈正相关。此外，ATG5水平较高的病例的无病生存（DFS）和总生存（OS）较低。多变量分析显示，ATG5的过表达预测了较差的OS和DFS。进一步的分析显示，在年轻患者和单发肿瘤数量亚组中，ATG5水平较高的病例的OS和DFS较差。示意图模型表明，标识图预测和实际情况具有一致性。综上所述，这些发现揭示了ATG5促进HCC的进展，使其成为肝细胞癌的潜在生物标志物和治疗靶点。本文受版权保护，版权所有。

As an critical component of the autophagic machinery, autophagy-related gene 5 (ATG5) is essential for autophagosome formation. Autophagy participates in various malignant tumor transformation and progression, but the role of ATG5 involved in hepatocellular carcinoma (HCC) remains to be illustrated.The expression of ATG5 was evaluated in 89 pairs of liver tumor and adjacent normal tissues. The correlation between ATG5 expression and clinicopathological characteristics or prognosis were evaluated. Moreover, clinical special analysis was conducted in the young patients group and the old patients group respectively, and nomograms estimating overall survival and disease-free survival were investigated.Our study demonstrated that the ATG5 level was increased in tumor specimens than adjacent normal tissues. Upregulated ATG5 level had positive association with serum α-fetoprotein (AFP). Moreover, cases with higher ATG5 level had poorer disease-free survival (DFS) and overall survival (OS) than those with lower ATG5 level. Multivariate analysis showed that overexpression of ATG5 predicts poor OS and DFS. Further analysis indicated that cases with higher ATG5 level had poorer OS and DFS in the young patients and solitary tumor number subgroup. The nomogram models suggested that it had a coherence between nomogram prediction and actual situation.Together these findings revealed that ATG5 promotes progression of HCC, making it a potentially biomarker in diagnosis and therapeutic target of hepatocellular carcinoma. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.