Abstract
Glycogen branching enzyme (GBE1) is a critical gene that participates in regulating glycogen metabolism. However, the correlations between GBE1 expression and the prognosis and tumor-associated macrophages in lung adenocarcinoma (LUAD) also remain unclear. Herein, we firstly analyzed the expression level of GBE1 in LUAD tissues and adjacent lung tissues via The Cancer Genome Atlas (TCGA) database. The effect of GBE1 on prognosis was estimated by utilizing TCGA database and the PrognoScan database. The relationships between the clinical characteristics and GBE1 expression were evaluated via TCGA database. We then investigated the relationships between GBE1 and infiltration of immune cells in LUAD by utilizing the CIBERSORT algorithm and Tumor Immune Estimation Resource (TIMER) database. In addition, we used a tissue microarray (TMA) containing 92 LUAD tissues and 88 adjacent lung tissues with immunohistochemistry staining to verify the association between GBE1 expression and clinical characteristics, as well as the immune cell infiltrations. We found the expression level of GBE1 was significantly higher in LUAD tissues. High expression of GBE1 was associated with poorer overall survival (OS) in LUAD. In addition, high expression of GBE1 was correlated with advanced T classification, N classification, M classification, TNM stage, and lower grade. Moreover, GBE1 was positively correlated with infiltrating levels of CD163+ tumor-associated macrophages in LUAD. In conclusion, the expression of GBE1 is associated with the prognosis and CD163+ tumor-associated macrophage infiltration in LUAD, suggesting that it has potential to be prognostic and immunological biomarkers in LUAD.
Highlights
Glycogen metabolism is an important part of the metabolic adaptation mechanisms used by cancer cells to adapt to the tumor microenvironment [1, 2]
The results showed that glycogen branching enzyme (GBE1) expression in lung adenocarcinoma (LUAD) tissues was higher than the adjacent tissues (Table 1)
We firstly found that GBE1 expression was higher in LUAD tissues when compared to normal tissues by utilizing The Cancer Genome Atlas (TCGA) database
Summary
Glycogen metabolism is an important part of the metabolic adaptation mechanisms used by cancer cells to adapt to the tumor microenvironment [1, 2]. Previous studies demonstrated that hypoxia-induced GBE1 expression could promote tumor progression through metabolic reprogramming in lung adenocarcinoma (LUAD) [5]. As an important part of tumor microenvironment, tumor-associated macrophages (TAMs) have been reported that they could affect the prognosis and efficacy of chemotherapy and immunotherapy [11,12,13,14,15,16,17]. Previous studies demonstrated that M0 and M2 macrophages, as well as resting memory CD4+ T cells, accounted for the majority of tumor-infiltrating immune cells in LUAD patients [20]. The tumor islet-infiltrating CD163+ tumor-associated macrophages were associated with the prognosis of nonsmall-cell lung cancer (NSCLC) patients [22]. Further analysis of the interaction between M2 TAMs and LUAD is urgently needed
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