METHODS: We performed a gene expression and survival analysis based on the human cancer genome atlas database of ccRCC patients (TCGA-KIRC).
RESULTS: The patients in the TCGA-KIRC (n = 537) were divided into two subgroups: NAA10-low and NAA10-high expression groups. NAA10-high ccRCC exhibited higher T stages (p = 0.002), a higher frequency of distant metastasis (p = 0.018), more advanced AJCC stages (p < 0.001), a lower overall survival time (p = 0.036), and a lower survival rate (p < 0.001). NAA10-high ccRCC was associated with increased activity of non-specific oncogenic pathways, including oxidative phosphorylation (p < 0.001) and cell cycle progression [G2 to M phase transition (p = 0.045) and E2F targets (p < 0.001)]. Additionally, the NAA10-high tumors showed reduced apoptosis via TRIAL pathways (p < 0.001) and increased levels of activity that promoted epithelial-mesenchymal transition (p = 0.026) or undifferentiation (p = 0.01). In ccRCC, NAA10 expression was found to be a negative prognostic factor in both non-metastatic (p < 0.001) and metastatic tumors (p = 0.032).
CONCLUSIONS: In ccRCC, NAA10 expression was shown to be a negative prognostic factor related to tumor progression rather than tumor initiation, and high NAA10 expression promoted epithelial-mesenchymal transition and undifferentiation.
方法:我们基于ccRCC患者的人类癌症基因组图谱数据库(TCGA-KIRC)进行了基因表达和生存分析。
结果:TCGA-KIRC患者(n=537)分为两个亚组:NAA10低表达组和NAA10高表达组。NAA10高ccRCC表现出更高的T阶段(p=0.002),远处转移的频率较高(p=0.018),更高级的AJCC阶段(p<0.001),较低的总生存时间(p=0.036),和较低的存活率(p<0.001)。NAA10高ccRCC与非特异性致癌途径的活性增加有关,包括氧化磷酸化(p<0.001)和细胞周期进程[G2至M期转变(p=0.045)和E2F目标(p<0.001)]。此外,高NAA10的肿瘤显示通过TRIAL途径的细胞凋亡减少(p<0.001),促进上皮-间质转化(p=0.026)或未分化(p=0.01)的活性水平增加.在ccRCC中,发现NAA10表达在非转移性(p<0.001)和转移性肿瘤(p=0.032)中均为负预后因素。
结论:在ccRCC中,NAA10表达被证明是与肿瘤进展有关的负预后因素,而不是肿瘤的发生。高表达NAA10促进上皮-间质转化和未分化。