CircRNA ZKSCAN1 promotes lung adenocarcinoma progression by miR‐185‐5p/TAGLN2 axis.

Background: Circ‐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. Methods: Levels 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. Results: Circ‐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. Conclusion: Circ‐ZKSCAN1 promoted LUAD tumorigenesis and DDP resistance by regulating miR‐185‐5p/TAGLN2 axis. [ABSTRACT FROM AUTHOR]