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dc.contributor.authorCheng, Yang
dc.contributor.authorHou, Kezuo
dc.contributor.authorWang, Yizhe
dc.contributor.authorChen, Yang
dc.contributor.authorZheng, Xueying
dc.contributor.authorQi, Jianfei
dc.contributor.authorYang, Bowen
dc.contributor.authorTang, Shiying
dc.contributor.authorHan, Xu
dc.contributor.authorShi, Dongyao
dc.contributor.authorWang, Ximing
dc.contributor.authorLiu, Yunpeng
dc.contributor.authorHu, Xuejun
dc.contributor.authorChe, Xiaofang
dc.date.accessioned2021-07-14T16:41:09Z
dc.date.available2021-07-14T16:41:09Z
dc.date.issued2021-06-24
dc.identifier.urihttp://hdl.handle.net/10713/16183
dc.description.abstractBackground: Lung adenocarcinoma (LUAD) is the most common pathological type of lung cancer, with high incidence and mortality. To improve the curative effect and prolong the survival of patients, it is necessary to find new biomarkers to accurately predict the prognosis of patients and explore new strategy to treat high-risk LUAD. Methods: A comprehensive genome-wide profiling analysis was conducted using a retrospective pool of LUAD patient data from the previous datasets of Gene Expression Omnibus (GEO) including GSE18842, GSE19188, GSE40791 and GSE50081 and The Cancer Genome Atlas (TCGA). Differential gene analysis and Cox proportional hazard model were used to identify differentially expressed genes with survival significance as candidate prognostic genes. The Kaplan-Meier with log-rank test was used to assess survival difference. A risk score model was developed and validated using TCGA-LUAD and GSE50081. Additionally, The Connectivity Map (CMAP) was used to predict drugs for the treatment of LUAD. The anti-cancer effect and mechanism of its candidate drugs were studied in LUAD cell lines. Results: We identified a 5-gene signature (KIF20A, KLF4, KRT6A, LIFR and RGS13). Risk Score (RS) based on 5-gene signature was significantly associated with overall survival (OS). Nomogram combining RS with clinical pathology parameters could potently predict the prognosis of patients with LUAD. Moreover, gliclazide was identified as a candidate drug for the treatment of high-RS LUAD. Finally, gliclazide was shown to induce cell cycle arrest and apoptosis in LUAD cells possibly by targeting CCNB1, CCNB2, CDK1 and AURKA.en_US
dc.description.urihttps://doi.org/10.3389/fonc.2021.665276en_US
dc.language.isoenen_US
dc.publisherFrontiers Media S.A.en_US
dc.relation.ispartofFrontiers in Oncologyen_US
dc.rightsCopyright © 2021 Cheng, Hou, Wang, Chen, Zheng, Qi, Yang, Tang, Han, Shi, Wang, Liu, Hu and Che.en_US
dc.subjectdrug repositioningen_US
dc.subjectgliclazideen_US
dc.subjectlung adenocarcinomaen_US
dc.subjectprognosisen_US
dc.subjectsignatureen_US
dc.titleIdentification of Prognostic Signature and Gliclazide as Candidate Drugs in Lung Adenocarcinomaen_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fonc.2021.665276
dc.identifier.pmid34249701
dc.source.volume11
dc.source.beginpage665276
dc.source.endpage
dc.source.countrySwitzerland


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