Abstract
Gastric cancer (GC) is one of the most widely occurring malignancies worldwide. Although the diagnosis and treatment strategies of GC have been greatly improved in the past few decades, the morbidity and lethality rates of GC are still rising due to lacking early diagnosis strategies and powerful treatments. In this study, a total of 37 differentially expressed genes were identified in GC by analyzing TCGA, GSE118897, GSE19826, and GSE54129. Using the PPI database, we identified 17 hub genes in GC. By analyzing the expression of hub genes and OS, MFAP2, BGN, and TREM1 were related to the prognosis of GC. In addition, our results showed that higher levels of BGN exhibited a significant correlation with shorter OS time in GC. Nomogram analysis showed that the dysregulation of BGN could predict the prognosis of GC. Moreover, we revealed that BGN had a markedly negative correlation with B cells but had positive correlations with CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells in GC samples. The pan-cancer analysis demonstrated that BGN was differentially expressed and related to tumor-infiltrating immune cells across human cancers. This study for the first time comprehensively revealed that BGN was a potential biomarker for the prediction of GC prognosis and tumor immune infiltration.
Highlights
Gastric cancer (GC) ranks fifth amid the widely occurring malignancies worldwide and is the third primary inducer of carcinoma-related mortality [1]
We found that 37 genes among these overlapped differentially expressed genes (DEGs) were differentially expressed in 4 datasets, including MFSD4A, ERO1B, DNER, CA9, TMED6, CPA2, GUCA2B, GKN1, CAPN13, MAMDC2, ZBTB16, MFAP2, BGN, THY1, THBS2, TIMP1, PRRX1, TMEM158, CLDN1, SALL4, SFRP4, TEAD4, RARRES1, CEMIP, EPHB2, CD300LF, PLPPR4, GREM1, FJX1, CHI3L1, IGF2BP3, WNT2, TREM1, CXCL9, CXCL8, and TREM2 (Figure 1(e))
By analyzing the correlation between Overall Survival (OS) and gene expression of hub genes using KM methods, we identified that MFAP2, BGN, and TREM1 levels were obviously correlated with OS time in GC
Summary
Gastric cancer (GC) ranks fifth amid the widely occurring malignancies worldwide and is the third primary inducer of carcinoma-related mortality [1]. Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV) are the main risk factors for GC development [1, 2]. The genetic diffuse GC accounts for approximately 1-3% of GC cases [7]. Host factors such as cytokine gene polymorphisms and bacterial factors are related to the increase in inflammation intensity and progression risk [8, 9]. Detection and diagnosis of GC at the early stage, is not easy, leading to an obvious decline in the survival rate after diagnosis [14].
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