Institute of Health Service and Transfusion Medicine, Beijing, 100850, People's Republic of China.
Beijing Key Laboratory of Blood Safety and Supply Technologies, Beijing, 100850, People's Republic of China.
Sci Rep. 2022 Apr 29;12(1):7006. doi: 10.1038/s41598-022-11050-w.
Adenocarcinoma of the pancreas (PAAD) is a cancerous growth that deteriorates rapidly and has a poor prognosis. Researchers are investigating autophagy in PAAD to identify a new biomarker and treatment target. An autophagy-related gene (ARG) model for overall survival (OS) was constructed using multivariate Cox regression analyses. A cohort of the Cancer Genome Atlas (TCGA)-PAAD was used as the training group as a basis for model construction. This prediction model was validated with several external datasets. To evaluate model performance, the analysis with receiver operating characteristic curves (ROC) was performed. The Human Protein Atlas (HPA) and Cancer Cell Line Encyclopedia (CCLE) were investigated to validate the effects of ARGs expression on cancer cells. Comparing the levels of immune infiltration between high-risk and low-risk groups was finished through the use of CIBERSORT. The differentially expressed genes (DEGs) between the low-/high-risk groups were analyzed further via Gene Ontology biological process (GO-BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, which were used to identify potential small-molecule compounds in Connectivity Map (CMap), followed by half-maximal inhibitory concentration (IC50) examination with PANC-1 cells. The risk score was finally calculated as follows: BAK1 × 0.34 + ITGA3 × 0.38 + BAG3 × 0.35 + APOL1 × 0.26-RAB24 × 0.67519. ITGA3 and RAB24 both emerged as independent prognostic factors in multivariate Cox regression. Each PAAD cohort had a significantly shorter OS in the high-risk group than in the low-risk group. The high-risk group exhibited infiltration of several immune cell types, including naive B cells (p = 0.003), plasma cells (p = 0.044), and CD8 T cells (nearly significant, p = 0.080). Higher infiltration levels of NK cells (p = 0.025), resting macrophages (p = 0.020), and mast cells (p = 0.007) were found in the high-risk group than the low-risk group. The in vitro and in vivo expression of signature ARGs was consistent in the CCLE and HPA databases. The top 3 enriched Gene Ontology biological processes (GO-BPs) were signal release, regulation of transsynaptic signaling, and modulation of chemical synaptic transmission, and the top 3 enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were MAPK, cAMP, and cell adhesion molecules. Four potential small-molecule compounds (piperacetazine, vinburnine, withaferin A and hecogenin) that target ARGs were also identified. Taking the results together, our research shows that the ARG signature may serve as a useful prognostic indicator and reveal potential therapeutic targets in patients with PAAD.
胰腺导管腺癌(PAAD)是一种恶性肿瘤,病情迅速恶化,预后不良。研究人员正在研究 PAAD 中的自噬,以确定新的生物标志物和治疗靶点。使用多变量 Cox 回归分析构建了用于总体生存(OS)的自噬相关基因(ARG)模型。癌症基因组图谱(TCGA)-PAAD 队列被用作训练组,作为模型构建的基础。使用多个外部数据集验证了该预测模型。为了评估模型性能,进行了接收器操作特征曲线(ROC)分析。通过人类蛋白质图谱(HPA)和癌症细胞系百科全书(CCLE)验证 ARG 表达对癌细胞的影响。通过 CIBERSORT 使用免疫浸润的高低风险组之间的水平进行比较。通过基因本体论生物过程(GO-BP)和京都基因与基因组百科全书(KEGG)分析进一步分析低/高风险组之间的差异表达基因(DEGs),用于识别 Connectivity Map(CMap)中的潜在小分子化合物,然后用 PANC-1 细胞进行半最大抑制浓度(IC50)检查。最后计算风险评分如下:BAK1×0.34+ITGA3×0.38+BAG3×0.35+APOL1×0.26-RAB24×0.67519。多变量 Cox 回归分析显示,ITGA3 和 RAB24 均为独立预后因素。在每个 PAAD 队列中,高风险组的 OS 明显短于低风险组。高风险组显示出几种免疫细胞类型的浸润,包括幼稚 B 细胞(p=0.003)、浆细胞(p=0.044)和 CD8 T 细胞(接近显著,p=0.080)。高风险组中 NK 细胞(p=0.025)、静止巨噬细胞(p=0.020)和肥大细胞(p=0.007)的浸润水平更高。CCLE 和 HPA 数据库中一致观察到特征性 ARG 的体外和体内表达。前 3 个富集的基因本体论生物过程(GO-BP)是信号释放、突触传递的调节和化学突触传递的调节,前 3 个富集的京都基因与基因组百科全书(KEGG)途径是 MAPK、cAMP 和细胞粘附分子。还确定了四种针对 ARG 的潜在小分子化合物(哌嗪、vinburnine、withaferin A 和 hecogenin)。综上所述,我们的研究表明,ARG 特征可能是一种有用的预后指标,并揭示了 PAAD 患者的潜在治疗靶点。