Affiliation:
1. Department of Thoracic Surgery Zigong Third People's Hospital Zigong China
Abstract
AbstractBackgroundCirc‐ZKSCAN1 has been found to accelerate non‐small cell lung cancer (NSCLC) progression; however, the role and mechanism of circ‐ZKSCAN1 in lung adenocarcinoma (LUAD) cisplatin (DDP) resistance remain unclear.MethodsLevels of genes and proteins were examined using qRT‐PCR. Functional experiments were performed using CCK‐8 assay, flow cytometry, transwell assay and xenograft model assay, respectively. Glucose metabolism was calculated by detecting glucose consumption, lactate production, ATP and HK‐2 levels. The interaction between miR‐185‐5p and circ‐ZKSCAN1 or transgelin 2 (TAGLN2) was validated by dual‐luciferase reporter assay.ResultsCirc‐ZKSCAN1 was highly expressed in DDP‐resistant LUAD tissues and cell lines, and circ‐ZKSCAN1 knockdown weakened DDP resistance and suppressed cell viability, migration, invasion, and glycolysis in LUAD. Circ‐ZKSCAN1 acted as a sponge of miR‐185‐5p, and the regulatory effects of circ‐ZKSCAN1 knockdown on LUAD were reversed by miR‐185‐5p downregulation. Meanwhile, miR‐185‐5p directly targeted TAGLN2, and performed anticancer effects by regulating TAGLN2. Importantly, silencing of circ‐ZKSCAN1 hindered tumor growth and promoted DDP sensitivity in vivo via regulating miR‐185‐5p and TAGLN2.ConclusionCirc‐ZKSCAN1 promoted LUAD tumorigenesis and DDP resistance by regulating miR‐185‐5p/TAGLN2 axis.
Subject
Pulmonary and Respiratory Medicine,Oncology,General Medicine
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献