
Prognostic and predictive values of CDK1 and MAD2L1 in lung adenocarcinoma
Author(s) -
Yuan-Xiang Shi,
Tao Zhu,
Ting Zou,
Wei Zhuo,
Yixin Chen,
Ma-Sha Huang,
Wei Zheng,
Chenjing Wang,
Xi Li,
XiaoYuan Mao,
Wei Zhang,
HongHao Zhou,
JiYe Yin,
ZhaoQian Liu
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.13252
Subject(s) - lung cancer , mad2 , medicine , carcinogenesis , cancer , adenocarcinoma , oncology , cancer research , cyclin dependent kinase 1 , biomarker , cell cycle , cell cycle checkpoint , biology , genetics
Lung cancer remains as the leading cause of cancer-related death worldwide, and lung adenocarcinoma (LUAD) is the most common histological subtype. This study aims to investigate biomarkers associated with cancer progression and prognosis of LUAD. We integrated expression profiles of 668 lung cancer patients in five datasets from the Gene Expression Omnibus (GEO) and identified a panel of differentially expressed genes (DEGs). Function enrichment analysis highlighted that these genes were closely associated with the carcinogenesis of LUAD, such as cell cycle, ECM-receptor interaction and p53 signaling pathway. Cyclin-dependent kinase 1 (CDK1) and MAD2 mitotic arrest deficient-like 1 (MAD2L1), two critical mitotic checkpoint genes, were selected for further study. Elevated expression of CDK1 and MAD2L1 was validated in an independent LUAD cohort. Kaplan-Meier analysis revealed that CDK1 and MAD2L1 expression was negatively correlated with both overall survival (OS) and relapse-free survival (RFS). In conclusion, CDK1 and MAD2L1 were adverse prognostic biomarkers for LUAD whose increased expression could render patients with LUAD a high risk of cancer recurrence and poor survival, suggesting that they might be applied as potential targets for LUAD treatment.