Introduction:Hepatocellular carcinoma (HCC) is a global health problem with increasing morbidity and mortality, and exploring the diagnosis and treatment of HCC at the gene level has be-come a research hotspot in recent years. As the rate-limiting enzyme of carnosine hydrolysis, CNDP1 participates in the progress of many diseases, but its function in HCC has not been fully elucidated.Methods:This study firstly screened differentially expressed genes from the biochip related to HCC by bioinformatic analysis, and CNDP1 was finally selected for in-depth study. Then the bioinformatics analysis results were validated by detecting the expression of CNDP1 in human HCC samples and he-patoma cell lines. Furthermore, the effect of CNDP1 on the malignant behavior of hepatoma cell lines were assessed using MTT colorimetric assay, EdU staining assay, colony formation, wound-healing assay and transwell, and the molecular mechanism was also preliminarily explored.Results:This study found that CNDP1 expression was decreased significantly in human HCC tissues and cell lines, and its overexpression could significantly suppress cell proliferation, migration and in-vasion of hepatoma cell lines. Mechanistically the GeneMANIA database predicted that CNDP1 could interact with various proteins involved in regulating PI3K-AKT-mTOR signaling pathway. Further-more, this study showed that CNDP1 overexpression could effectively inhibit the activation of PI3K-AKT-mTOR signaling pathways, more significantly, inhibition of PI3K-AKT-mTOR signaling path-way could disrupt the anti-cancer effect of CNDP1 on HCC.Conclusion:This study confirm that CNDP1 expression is decreased significantly in HCC, and has potential anti-cancer activity, this discovery provides a cytological basis for further understanding the biological function of CNDP1 and diagnosis and gene therapy of HCC in the future.