Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high morbidity and mortality. Therefore, it is very important to find potential biomarkers that can effectively predict the prognosis and progression of HCC. Recent studies have shown that anti-silencing function 1B (ASF1B) may be a new proliferative marker for tumor diagnosis and prognosis. However, the expression and function of ASF1B in hepatocellular carcinoma remain to be determined. In this study, integrated analysis of the Cancer Genome Atlas (TCGA), genotypic tissue expression (GTEx), and Gene Expression Omnibus (GEO) databases revealed that ASF1B was highly expressed in HCC. Kaplan-Meier survival curve showed that elevated ASF1B expression was associated with poor survival in patients with liver cancer. Correlation analysis of immune infiltration suggested that ASF1B expression was significantly correlated with immune cell infiltration in HCC patients. Gene set enrichment analysis (GSEA) indicated that ASF1B regulated the cell cycle, DNA Replication and oocyte meiosis signaling. Our experiments confirmed that ASF1B was highly expressed in HCC tissues and HCC cell lines. Silence of ASF1B inhibited hepatocellular carcinoma cell growth in vitro. Furthermore, ASF1B deficiency induced apoptosis and cell cycle arrest. Mechanistically, ASF1B knockdown reduced the expression of proliferating cell nuclear antigen (PCNA), cyclinB1, cyclinE2 and CDK9.Moreover, ASF1B interacted with CDK9 in HCC cells. Taken together, these results suggest that the oncogenic gene ASF1B could be a target for inhibiting hepatocellular carcinoma cell growth.
Highlights
In global cancer statistics, the incidence of liver cancer ranks sixth and the mortality rate ranks third
The results showed that anti-silencing function 1B (ASF1B) was highly expressed in most tumors, and only a few tumors showed low expression (Figure 1A)
Through the mining of genotypic tissue expression (GTEx) and the Cancer Genome Atlas (TCGA) databases, we found that ASF1B was highly expressed in a variety of tumors, including Cholangiocarcinoma (CHOL), Colon adenocarcinoma (COAD), Esophageal carcinoma (ESCA), Liver hepatocellular carcinoma (LIHC), Pancreatic adenocarcinoma (PADD), Rectum adenocarcinoma(READ), Stomach adenocarcinoma(STAD) (Figure 1B)
Summary
The incidence of liver cancer ranks sixth and the mortality rate ranks third. In 2020, according to statistics, there are 905,677 new cases of liver cancer worldwide. It is estimated that by 2025, the incidence of liver cancer will exceed 1 million cases, which is a serious threat to human life and health [1,2,3]. Hepatocellular carcinoma (HCC), known as liver hepatocellular. Oncogene ASF1B Influenced Proliferation in HCC carcinoma (LIHC), is responsible for 90% of all liver cancers [4]. Clinical HCC treatments, including surgery, interventional therapy, radiotherapy, chemotherapy and immunotherapy, are usually performed, have been significant improvements. There is an urgent need to identify and develop new molecular targets for hepatocellular carcinoma therapy
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