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作 者:YANG ZHANG LIXIA MA TINGTING ZHANG PEIDONG LI JIABIN XU ZHUO WANG
机构地区:[1]Department of Oncology,Jilin Province Cancer Hospital,Jilin,130012,China
出 处:《Oncology Research》2021年第2期129-139,共11页肿瘤学研究(英文)
基 金:supported by Jilin Province Cancer Hospital.
摘 要:In this study,we mainly focus on probing expression profile and detailed functions of long non-coding RNA TFAP2A antisense RNA 1(TFAP2A-AS1)in non-small cell lung cancer(NSCLC).Moreover,the mechanisms played by TFAP2A-AS1 were unraveled comprehensively.Herein,a notable overexpressed TFAP2A-AS1 in NSCLC was observed by TCGA and our own cohort.An increased TFAP2A-AS1 level displayed a negative correlation with the overall survival of patients with NSCLC.Loss-of-function approaches illustrated that the absence of TFAP2A-AS1 weakened NSCLC cell proliferation,colony formation,migration and invasion in vitro.Also,interference of TFAP2A-AS1 caused in vivo tumor growth suppression.Mechanistically,TFAP2A-AS1 could negative regulate microRNA-584-3p(miR-584-3p)as a competitive endogenous RNA.Furthermore,cyclin-dependent kinase 4(CDK4),a direct target of miR-584-3p,was positively controlled by TFAP2A-AS1 in a miR-5184-3p-dependent manner.Rescue function experiments corroborated that the anticancer activities of TFAP2A-AS1 deficient on the oncogenicity of NSCLC cells were reversed by downregulating miR-584-3p or overexpressing CDK4.To sum up,TFAP2A-AS1 exhibits cancerpromoting roles in NSCLC through the adjustment of miR-584-3p/CDK4 axis.
关 键 词:TFAP2A antisense RNA 1 Lung cancer ceRNA pathway Therapeutic target
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