Zhang Qun-Xian, Yang Ye, Yang Heng, Guo Qiang, Guo Jia-Long, Liu Hua-Song, Zhang Jun, Li Dan
Department of Cardiothoracic Surgery, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Department of Psychiatry, Traditional Chinese Medicine Hospital of Shiyan, Shiyan, China.
Transl Cancer Res. 2021 Oct;10(10):4413-4431. doi: 10.21037/tcr-21-1431.
The abnormal expression of deoxyribonucleic acid (DNA) repair genes might be the cause of tumor development and resistance of malignant cells to chemotherapeutic drugs. A risk model based on the X-ray repair of cross-complementary () genes was constructed to improve the diagnosis and treatment of lung adenocarcinoma (LUAD) patients.
The expression levels, diagnostic values, and prognostic values of genes were identified, and the roles and regulatory mechanisms of the risk model based on the 4/5/6 in LUAD progression was explored via The Cancer Genome Atlas (TCGA) and Oncomine databases.
, (), and () were overexpressed, and had diagnostic value for LUAD. The genes were involved in DNA repair, and participated in the regulation of non-homologous end-joining, homologous recombination, etc. The overall survival (OS), tumor (T) stage, and survival status of patients were significantly different between the Cluster1 and Cluster2 groups. were independent risk factors affecting the prognosis of LUAD patients. The risk score was related to the prognosis, sex, clinical stage, T, lymph node (N), and metastasis (M) stage, as well as the survival status of LUAD patients. The clinical stage and risk score were independent risk factors for poor prognosis in LUAD patients. The risk model was involved in RNA degradation, cell cycle, basal transcription factors, DNA replication etc. The risk scores were significantly correlated with the expression levels of , , , , , , , , , and .
The risk model based on the 4/5/6 genes could predict the progression of LUAD patients.
脱氧核糖核酸（DNA）修复基因的异常表达可能是肿瘤发生及恶性细胞对化疗药物产生耐药性的原因。构建基于X射线修复交叉互补（）基因的风险模型，以改善肺腺癌（LUAD）患者的诊断和治疗。
确定基因的表达水平、诊断价值和预后价值，并通过癌症基因组图谱（TCGA）和Oncomine数据库探讨基于4/5/6的风险模型在LUAD进展中的作用和调控机制。
、（）和（）表达上调，对LUAD具有诊断价值。这些基因参与DNA修复，参与非同源末端连接、同源重组等的调控。Cluster1组和Cluster2组患者的总生存期（OS）、肿瘤（T）分期和生存状态存在显著差异。是影响LUAD患者预后的独立危险因素。风险评分与LUAD患者的预后、性别、临床分期、T、淋巴结（N）和转移（M）分期以及生存状态相关。临床分期和风险评分是LUAD患者预后不良的独立危险因素。风险模型参与RNA降解、细胞周期、基础转录因子、DNA复制等过程。风险评分与、、、、、、、、和的表达水平显著相关。
基于4/5/6基因的风险模型可预测LUAD患者的病情进展。
