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Abstract：
Phosphodiesterase 4B (PDE4B) is a key enzyme involved in regulating intracellular cyclic adenosine monophosphate levels and plays a significant role in the diagnosis, classification, treatment, and prognosis of various cancers. However, the role of PDE4B in gastric cancer (GC) remains unclear. We used the GEPIA2 (Gene Expression Profiling Interactive Analysis 2) database to analyze the differential expression level of PDE4B across tumor samples and verified our findings via qPCR and immunohistochemical analysis. We also analyzed the correlation between PDE4B expression levels and clinical pathological parameters, and prognosis, in the database. The effects of PDE4B on GC proliferation, migration, and invasion were evaluated through in vitro and in vivo experiments. Enrichment analysis was performed using bioinformatic tools, and results were validated by western blot analysis. The correlation between PDE4B expression and immune cell infiltration was investigated using bioinformatics tools. PDE4B is highly expressed in GC and is significantly associated with deep infiltration, distant metastasis, tumor, node, metastasis (TNM) stage, and preoperative CA199 levels. Over-expression of PDE4B promotes proliferation, clonal formation, migration, and invasion of GC cells and is associated with poor prognosis. PDE4B promotes the infiltration of immune cells into the tumor microenvironment (TME) and the phosphorylation of PI3K/AKT pathway, increasing MYC expression. PDE4B can serve as an independent prognostic biomarker for GC. We found that PDE4B can promote immune cell infiltration of the TME and mediate malignancy in gastric cancer through the PI3K/AKT/MYC pathway.
摘要：
磷酸二酯酶4B(PDE4B)是参与调节细胞内环磷酸腺苷水平的关键酶,在诊断中发挥着重要作用。分类，治疗,和各种癌症的预后。然而,PDE4B在胃癌(GC)中的作用尚不清楚.我们使用GEPIA2(基因表达谱交互式分析2)数据库来分析肿瘤样品中PDE4B的差异表达水平,并通过qPCR和免疫组织化学分析验证我们的发现。我们还分析了PDE4B表达水平与临床病理参数之间的相关性。和预后，在数据库中。PDE4B对GC增殖的影响,迁移,通过体外和体内实验评估侵袭性。使用生物信息学工具进行富集分析，结果通过蛋白质印迹分析进行验证。使用生物信息学工具研究PDE4B表达与免疫细胞浸润之间的相关性。PDE4B在GC中高表达，与深层浸润显著相关，远处转移,肿瘤，节点,转移（TNM）分期，术前CA199水平。PDE4B的过表达促进增殖，克隆形成，迁移,和GC细胞的侵袭，并与预后不良有关。PDE4B促进免疫细胞向肿瘤微环境(TME)的浸润和PI3K/AKT通路的磷酸化,增加MYC表达。PDE4B可以作为GC的独立预后生物标志物。我们发现PDE4B可以通过PI3K/AKT/MYC途径促进TME的免疫细胞浸润并介导胃癌的恶性。
