Abstract
Purpose This study was performed to investigate the association of CEP55 expression with liver cancer and explore potential underlying mechanisms. Materials and Methods. Data obtained from The Cancer Genome Atlas (TCGA) was used to investigate CEP55 expression, its prognostic value, the potential mechanisms of its upregulation, CEP55-related pathways, and its biological functions in liver cancer. Data from Gene Expression Omnibus (GEO) and International Cancer Genome Consortium (ICGC) was used to validate survival analysis. The correlation between CEP55 and tumor-infiltrating immune cells (TIICs) in liver cancer was determined by using Tumor Immune Estimation Resource (TIMER). Results CEP55 was significantly overexpressed in the liver tumor sample compared to the adjacent normal liver sample. High CEP55 expression was significantly associated with histological grade, advanced stages, histological type, high T classification, and survival status. High CEP55 expression was significantly related to dismal prognosis compared with low CEP55 expression, which was validated by the GSE54236 dataset and ICGC database. Meanwhile, CEP55 was identified as the risk factor to independently predict overall survival (OS) for patients with liver cancer upon multivariate analysis. Enrichment analysis indicated that cell cycle, DNA replication, pathways in cancer, mTOR signaling pathway, and VEGF signaling pathway were significantly enriched in the high CEP55 expression group. In addition, the CEP55 expression was significantly related to the infiltration level of B cells, CD4+ T cells, CD8+ T cells, macrophages, neutrophils, and dendritic cells in hepatocellular carcinoma (HCC). CEP55 methylation level was negatively correlated to its mRNA expression. And patients with CEP55 hypermethylation and low expression can achieve a better prognosis than those with CEP55 hypomethylation and high expression. Conclusion CEP55 may serve as a candidate treatment target for it is a determinant of prognosis and immune infiltration in liver cancer patients. DNA hypomethylation might contribute to the overexpression of CEP55 in liver cancer.
Highlights
Liver cancer ranks the 6th place in terms of global tumor incidence, and it is the 4th leading cause of cancer-related deaths [1]
Growing evidence showed that tumor immune environment is related to the prognosis in various cancers; we further explored the correlation between tumor-infiltrating immune cells (TIICs) and Centrosome protein 55 (CEP55)
The results indicated that CEP55 expression was significantly related to the infiltration level of B cells (R = 0:475, p = 1:02e − 20), CD4+ T cells (R = 0:345, p = 4:57e − 11), CD8+ T cells (R = 0:367, p = 2:44e − 12), macrophages (R = 0:5, p = 6:20e − 23), neutrophils (R = 0:345, p = 4:53e − 13), and dendritic cells (R = 0:473, p = 2:37e − 20) in Hepatocellular carcinoma (HCC) (Figure 10(b))
Summary
Liver cancer ranks the 6th place in terms of global tumor incidence, and it is the 4th leading cause of cancer-related deaths [1]. Hepatocellular carcinoma (HCC), one of the frequently seen primary liver tumors, occupies about 80% of liver cancers, followed by cholangiocarcinoma (CCA), accounting for approximately 15%. The highest liver cancer morbidity is reported in Asia and Africa. 75% of liver cancer occurs in Asia, and China accounts for more than half of the total cases in the world. Aflatoxin exposure and chronic hepatitis B virus (HBV) infection are two major risk factors reported across most high-incidence countries in Asia and Africa [2]. Liver cancer has become the second most fatal tumor after pancreatic cancer with a 5-year survival rate of 18% [3]. Finding reliable predictors and potential therapeutic targets involved in the occurrence and development of liver cancer is urgently needed
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