Abstract
Recent research has indicated that metabolically related genes play crucial roles in the pathogenesis of hepatocellular carcinoma (HCC). We evaluated the associations between novel biomarkers and retinol-binding protein 4 (RBP4) for predicting clinical HCC outcomes, hub-related genes, pathway regulation, and immune cells infiltration. Bioinformatic analyses based on data from The Cancer Genome Atlas were performed using online analysis tools. RBP4 expression was low in HCC and was also down-regulated in pan-cancers compared with normal tissues. RBP4 expression was also significantly different based on age (41–60 years old versus 61–80 years old), and low RBP4 expression levels were associated with advanced tumor stages and grades. Higher RBP4 expression was associated with better overall survival time in HCC patients, and we identified a deletion-mutation rate of 1.4% in RBP4. We also identified ten co-expressed genes most related to RBP4 and explored the relationships between six hub genes (APOB, FGA, FGG, SERPINC1, APOA1, and F2) involved in RBP4 regulation. A pathway enrichment analysis for RBP4 indicated complement and coagulation cascades, metabolic pathways, antibiotic biosynthesis pathways, peroxisome proliferator-activated receptor signaling pathways, and pyruvate metabolism pathways. These results suggest that RBP4 may be a novel biomarker for HCC prognosis, and an indicator of low immune response to the disease.
Highlights
Hepatocellular carcinoma (HCC) can occur after years of chronic liver disease and comprises more than 90% of primary liver cancers
We found that retinol-binding protein 4 (RBP4) protein expression was lower in HCC tissue, but was highly expressed in normal tissue (P
For the pan-cancers comparisons, we utilized TIMER to explored RBP4 expression, and the results showed that RBP4 was highly expressed in most normal tissues compared with its corresponding tumor tissues, including bladder urothelial carcinoma (BLCA), breast invasive carcinoma (BRCA), cholangiocarcinoma (CHOL), head and neck squamous cell carcinoma (HNSC), kidney chromophobe (KICH), kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC), prostate adenocarcinoma (PRAD), skin cutaneous melanoma (SKCM), and stomach adenocarcinoma (STAD)
Summary
Hepatocellular carcinoma (HCC) can occur after years of chronic liver disease and comprises more than 90% of primary liver cancers. HCC is the second leading cause of cancer-related deaths worldwide and is responsible for nearly 800,000 deaths annually [1,2]. Carcinogen-mediated molecular mechanisms are involved in the genesis of cancer and metabolically in the tumor-associated microenvironment [3]. Metabolic disorders are known to increase the risk of cancer and cancer-related mortality [4]. Metabolic alterations in tumor-microenvironments related to hyperinsulinemia and obesity are associated with an increased risk for, incidence of, and mortality from breast cancer [5], gastrointestinal cancer [6], lung cancer [7], prostate cancer [8], colorectal cancer [9], and pancreatic cancer [10].
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