Department of Respiratory, Qianjiang Central Hospital of Chongqing, Chongqing, 409000, People's Republic of China.
Department of Intensive Care Unit, Qianjiang Central Hospital of Chongqing, No.63, Chengxijiu Road, Qianjiang District, Chongqing, 409000, People's Republic of China.
World J Surg Oncol. 2022 Feb 8;20(1):32. doi: 10.1186/s12957-021-02477-y.
To investigate the role of transmembrane p24 trafficking protein 2 (TMED2) in lung adenocarcinoma (LUAD) and determine whether TMED2 knockdown could inhibit LUAD in vitro and in vivo.
TIMER2.0, Kaplan-Meier plotter, gene set enrichment analysis (GSEA), Target Gene, and pan-cancer systems were used to predict the potential function of TMED2. Western blotting and immunohistochemistry were performed to analyze TMED2 expression in different tissues or cell lines. The proliferation, development, and apoptosis of LUAD were observed using a lentivirus-mediated TMED2 knockdown. Bioinformatics and western blot analysis of TMED2 against inflammation via the TLR4/NF-κB signaling pathway were conducted.
TMED2 expression in LUAD tumor tissues was higher than that in normal tissues and positively correlated with poor survival in lung cancer and negatively correlated with apoptosis in LUAD. The expression of TMED2 was higher in tumors or HCC827 cells. TMED2 knockdown inhibited LUAD development in vitro and in vivo and increased the levels of inflammatory factors via the TLR4/NF-κB signaling pathway. TMED2 was correlated with TME, immune score, TME-associated immune cells, their target markers, and some mechanisms and pathways, as determined using the TIMER2.0, GO, and KEGG assays.
TMED2 may regulate inflammation in LUAD through the TLR4/NF-κB signaling pathway and enhance the proliferation, development, and prognosis of LUAD by regulating inflammation, which provide a new strategy for treating LUAD by regulating inflammation.
研究跨膜 p24 转运蛋白 2（TMED2）在肺腺癌（LUAD）中的作用，并确定 TMED2 敲低是否能在体外和体内抑制 LUAD。
使用 TIMER2.0、Kaplan-Meier plotter、基因集富集分析（GSEA）、靶基因和泛癌系统预测 TMED2 的潜在功能。使用 Western blot 和免疫组织化学分析不同组织或细胞系中 TMED2 的表达。通过慢病毒介导的 TMED2 敲低观察 LUAD 的增殖、发育和凋亡。通过 TLR4/NF-κB 信号通路对 TMED2 针对炎症的生物信息学和 Western blot 分析。
LUAD 肿瘤组织中 TMED2 的表达高于正常组织，与肺癌的不良生存呈正相关，与 LUAD 的细胞凋亡呈负相关。TMED2 在肿瘤或 HCC827 细胞中的表达较高。TMED2 敲低抑制 LUAD 的体外和体内发展，并通过 TLR4/NF-κB 信号通路增加炎症因子的水平。TMED2 与 TME、免疫评分、TME 相关免疫细胞、其靶标标志物以及一些机制和途径相关，这是通过 TIMER2.0、GO 和 KEGG 试验确定的。
TMED2 可能通过 TLR4/NF-κB 信号通路调节 LUAD 中的炎症，并通过调节炎症增强 LUAD 的增殖、发育和预后，为通过调节炎症治疗 LUAD 提供了一种新策略。
