Abstract
Gastric cancer is a disease characterized by inflammation, and epithelial-to-mesenchymal transition (EMT) and tumor-associated macrophages (TAMs) both play a vital role in epithelial-driven malignancy. In the present study, we performed an integrated bioinformatics analysis of transcriptome data from multiple databases of gastric cancer patients and worked on a biomarker for evaluating tumor prognosis. We found that cadherin 11 (CDH11) is highly expressed not only in gastric cancer tissues but also in EMT molecular subtypes and metastatic patients. Also, we obtained evidence that CDH11 has a significant correlation with infiltrating immune cells in the tumor microenvironment (TME). Our findings reflected that CDH11 likely plays an important role in tumor immune escape and could provide a prognostic biomarker and potential therapeutic target for patients with gastric cancer.
Highlights
Gastric cancer (GC) ranks fifth in global cancer incidence and is the third most significant contributor to cancerrelated mortality [1]
We explored the possible molecular mechanisms of cadherin 11 (CDH11) involved in gastric carcinogenesis via the construction of the protein-protein interaction (PPI) and the coexpression network on the STRING database [33] as well as investigation of the relationships between CDH11 and the levels of infiltrating cells in tumor microenvironment (TME) based on the TIMER database
Data obtained from TIMER and GEPIA showed similar results, with high levels of CDH11 expression shown to be more common in adenocarcinoma like breast, gastric, pancreatic, and colorectal cancers, while lower expression mainly existed in tumors of the urinary and respiratory systems (Figure 1(b) and Figure S1)
Summary
Gastric cancer (GC) ranks fifth in global cancer incidence and is the third most significant contributor to cancerrelated mortality [1]. During H. pylori infection, the host’s defense system launches an immune response aimed at annihilating bacterium, resulting in durable inflammation in the gastric mucosa followed by a series of pathological alterations that may become cancerous. In patients with gastritis without H. pylori infection, normal cells are repeatedly stimulated by chronic inflammation for a long time and gradually become dysfunctional with tumorigenic potential, in part via recruiting immune cells into the microenvironment [4]. All of this supports the view that GC is a disease dominated by inflammation [5]. To a certain extent, changes in TME composition, especially in the types of inflammatory infiltrating cells, might provide a better microenvironment for gastric mucosa cells to obtain the capability for carcinogenesis
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