Wang Zhe, Mu Lin, Feng He, Yao Jialin, Wang Qin, Yang Wenxiao, Zhou Huiling, Li Qinglin, Xu Ling
Department of Oncology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Department of Ophthalmology, Longhua Hospital Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Front Genet. 2022 Nov 24;13:993322. doi: 10.3389/fgene.2022.993322. eCollection 2022.
The purpose of this study was to explore platinum resistance-related biomarkers and mechanisms in lung adenocarcinoma. Through the analysis of gene expression data of lung adenocarcinoma patients and normal patients from The Cancer Genome Atlas, Gene Expression Omnibus database, and A database of genes related to platinum resistance, platinum resistance genes in lung adenocarcinoma and platinum resistance-related differentially expressed genes were obtained. After screening by a statistical significance threshold, a total of 252 genes were defined as platinum resistance genes with significant differential expression, of which 161 were up-regulated and 91 were down-regulated. The enrichment results of up-regulated gene Gene Ontology (GO) showed that TOP3 entries related to biological processes (BP) were double-strand break repair, DNA recombination, DNA replication, the down-regulated gene GO enriches the TOP3 items about biological processes (BP) as a response to lipopolysaccharide, muscle cell proliferation, response to molecule of bacterial origin. Gene Set Enrichment Analysis showed that the top three were e2f targets, g2m checkpoint, and rgf beta signaling. A prognostic model based on non-negative matrix factorization classification showed the characteristics of high- and low-risk groups. The prognostic model established by least absolute shrinkage and selection operator regression and risk factor analysis showed that genes such as HOXB7, NT5E, and KRT18 were positively correlated with risk score. By analyzing the differences in m6A regulatory factors between high- and low-risk groups, it was found that FTO, GPM6A, METTL3, and YTHDC2 were higher in the low-risk group, while HNRNPA2B1, HNRNPC, TGF2BP1, IGF2BP2, IGF2BP3, and RBM15B were higher in the high-risk group. Immune infiltration and drug sensitivity analysis also showed the gene characteristics of the platinum-resistant population in lung adenocarcinoma. ceRNA analysis showed that has-miR-374a-5p and RP6-24A23.7 were lower in the tumor expression group, and that the survival of the low expression group was worse than that of the high expression group. In conclusion, the results of this study show that platinum resistance-related differentially expressed genes in lung adenocarcinoma are mainly concentrated in biological processes such as DNA recombination and response to lipopolysaccharide. The validation set proved that the high-risk group of our prognostic model had poor survival. M6A regulatory factor analysis, immune infiltration, and drug sensitivity analysis all showed differences between high and low-risk groups. ceRNA analysis showed that has-miR-374a-5p and RP6-24A23.7 could be protective factors. Further exploration of the potential impact of these genes on the risk and prognosis of drug-resistant patients with lung adenocarcinoma would provide theoretical support for future research.
本研究的目的是探索肺腺癌中铂耐药相关的生物标志物和机制。通过对来自癌症基因组图谱、基因表达综合数据库以及一个铂耐药相关基因数据库的肺腺癌患者和正常患者的基因表达数据进行分析,获得了肺腺癌中的铂耐药基因以及铂耐药相关差异表达基因。经统计学显著性阈值筛选后,共确定了252个具有显著差异表达的铂耐药基因,其中161个上调,91个下调。上调基因的基因本体(GO)富集结果显示,与生物过程(BP)相关的前三项条目为双链断裂修复、DNA重组、DNA复制;下调基因的GO富集的关于生物过程(BP)的前三项条目为对脂多糖的反应、肌肉细胞增殖、对细菌来源分子的反应。基因集富集分析表明,前三位分别是e2f靶点、g2m检查点和rgfβ信号通路。基于非负矩阵分解分类的预后模型显示了高风险组和低风险组的特征。通过最小绝对收缩和选择算子回归及风险因素分析建立的预后模型表明,HOXB7、NT5E和KRT18等基因与风险评分呈正相关。通过分析高风险组和低风险组之间m6A调控因子的差异,发现低风险组中FTO、GPM6A、METTL3和YTHDC2较高,而高风险组中HNRNPA2B1、HNRNPC、TGF2BP1、IGF2BP2、IGF2BP3和RBM15B较高。免疫浸润和药物敏感性分析也显示了肺腺癌铂耐药人群的基因特征。ceRNA分析表明,肿瘤表达组中has-miR-374a-5p和RP6-24A23.7较低,低表达组的生存率低于高表达组。总之,本研究结果表明,肺腺癌中铂耐药相关差异表达基因主要集中在DNA重组和对脂多糖反应等生物过程中。验证集证明我们预后模型的高风险组生存率较差。m6A调控因子分析、免疫浸润和药物敏感性分析均显示高风险组和低风险组之间存在差异。ceRNA分析表明,has-miR-374a-5p和RP6-24A23.7可能是保护因子。进一步探索这些基因对肺腺癌耐药患者风险和预后的潜在影响,将为未来研究提供理论支持。