A comprehensive functional analysis indicates CNDP1 mitigates hepatocellular carcinoma and may be associated with immune cell infiltration and m6A-related genes

Author:

Wen Chong1,Shi Ruolin1,An Yulong2,Zhang Shuting2,Wang Tao1,Luo Hao1

Affiliation:

1. Southwest Jiaotong University

2. Affiliated Hospital of Southwest Jiaotong University, The General Hospital of Western Theater Command

Abstract

Abstract Background Carnosine dipeptidase 1 (CNDP1) is a member of the dipeptidase family that hydrolyzes the substrate L-sarcosine, and its relationship with hepatocellular carcinoma (HCC) has not been previously reported. We aim to explore the expression of CNDP1 in HCC and its relationship with prognosis. Methods Online analysis tools and the TCGA database were used to identify CNDP1 expression, correlation analysis, functional enrichment analysis, and patient prognosis analysis. Lentiviral transfection was used to construct two HCC cell lines (Sk-hep-1 and Huh-7) with high CNDP1 expression and knockdown. Transwell assay, wound healing assay, Cell proliferation assay, and subcutaneous xenograft assay were used to evaluate the invasion, migration, proliferation, and tumorigenesis of the experimental HCC cells, respectively. Results CNDP1 is down-regulated in HCC tissues, and low CNDP1 results in poor overall survival (OS) and disease-specific survival (DSS). The expression of CNDP1 was correlated with the infiltration level of various m6A-related genes and immune cells in HCC tissues. Cell and animal experiments confirmed that the expression of CNDP1 was decreased in Sk-hep-1 and Huh-7 HCC cell lines and the migration, proliferation, invasion, and tumor formation ability of HCC cell lines in the CNDP1-overexpression groups was weakened, while that in the knockdown groups was enhanced. Conclusion The decreased expression of CNDP1 in HCC suggests a worse prognosis and may be associated with immune cell infiltration and m6A-related genes. Our findings suggest that CNDP1 may be a new target for the diagnosis and treatment of HCC.

Publisher

Research Square Platform LLC

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