Abstract
Neuropeptide-associated fibroblast activation protein (FAP) may be an important risk factor for neurovascular metastasis in hepatocellular carcinoma. Analysis of The Cancer Genome Atlas (TCGA) database showed that FAP mRNA was highly expressed in most human tumor tissues. The HPA database then verified that FAP was highly expressed in tumor tissues following protein translation. Survival analysis then showed that the level of FAP expression significantly affected the overall survival (OS), progress free interval (PFI), and disease specific survival (DSS) of patients with hepatocellular carcinoma. A high expression of FAP in tumor tissue is associated with poor patient prognosis. According to the results of spearman correlation, AC009099 and FAP were negatively correlated with miR-7152 expression, while AC009099 and FAP expression were positively correlated. The lncRNA AC007099.1, which may serve as a potential target for the treatment of hepatocellular carcinoma, was associated with liver cancer. AC007099.1/miR-7152/FAP was found to be associated with immune infiltration in patients with hepatocellular carcinoma. Enrichment analysis suggests that the AC009099/miR-7152/FAP ceRNA regulatory network is associated with neuropeptide functional pathways. In conclusion, a neuropeptide-related AC009099/miR-7152/FAP ceRNA regulatory network was constructed in this study.
Highlights
Liver cancer is one of the deadliest cancers in the world, and 70% to 90% of primary liver cancers are hepatocellular carcinomas
The Cancer Genome Atlas (TCGA) database analysis shows that the fibroblast activation protein (FAP) gene is highly expressed in most human tumor tissues (Figure 1(a))
The HAP database verified the expression of FAP at the translational level and found that the protein was highly expressed in tumor tissues (Figure 1(b))
Summary
Liver cancer is one of the deadliest cancers in the world, and 70% to 90% of primary liver cancers are hepatocellular carcinomas. There is still a lack of effective treatments for hepatocellular carcinoma, except for physical and chemical treatments. These treatments include radiation, ablation, surgical resection, transplantation, and transcatheter arterial chemoembolization, while only a few expensive drugs have little effect [3, 4]. Tumor microenvironment helps cancer cells evade immune surveillance and supports their proliferation, metastasis, and dissemination [6–8]. The heterogeneity of hepatocellular carcinoma cells causes drug resistance in hepatocellular carcinoma, which serves as a major challenge in treating hepatocellular carcinoma. The cancer microenvironment is generally stable and rarely progresses to drug-resistant subtypes. It is much more favorable to select a component of the microenvironment as an antitumor target than a drug-resistant cancer cell
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