Circ_0058608 contributes to the progression and taxol resistance of non-small cell lung cancer by sponging miR-1299 to upregulate GBP1. Issue 1 (18th November 2022)

• Record Type: Journal Article
• Authors: Xuan, Xianglan; Wang, Zhiguang; Wang, Yayan
• Is Part Of: Anti-cancer drugs. Volume 34:Issue 1(2023)
• Page Start: 103
• Page End: 114
• Publication Date: 2022-11-18
• Subjects: circ_0058608 -- guanylate binding protein 1 -- miR-1299 -- nonsmall cell lung cancer -- taxol resistance; Antineoplastic agents -- Periodicals; Cancer -- Chemotherapy -- Periodicals; Antineoplastic Agents -- therapeutic use -- Periodicals; Drug Therapy -- Periodicals; 616.994061
• DOI: 10.1097/CAD.0000000000001346
• Languages: English
• ISSNs: 0959-4973

Abstract

Abstract : Circular RNAs (circRNAs) act as key regulators in human cancers and chemoresistance. Here, we aimed to explore the role and mechanism of circ_0058608 in nonsmall cell lung cancer (NSCLC) and taxol resistance. The expression of circ_0058608, microRNA-1299 (miR-1299) and guanylate binding protein 1 (GBP1) mRNA was determined by quantitative real-time PCR. In-vitro and in-vivo assays were conducted using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), colony formation, transwell assays, flow cytometry and animal xenograft experiments. The interaction between miR-1299 and circ_0058608 or GBP1 was confirmed by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0058608 was overexpressed in NSCLC tissues/cells and taxol-resistant NSCLC tissues/cells. Circ_0058608 knockdown inhibited NSCLC cell proliferation and metastasis and also suppressed tumor growth in vivo . Moreover, circ_0058608 knockdown increased taxol sensitivity by increasing taxol-induced apoptosis in taxol-resistant NSCLC cells. Moreover, circ_0058608 silencing enhanced taxol-induced tumor growth of NSCLC in vivo . MiR-1299 was a target of circ_0058608, and the effects of circ_0058608 knockdown on NSCLC cell progression and taxol resistance were reversed by miR-1299 inhibition. Additionally, miR-1299 could interact with GBP1, and miR-1299 suppressed NSCLC cell progression and taxol resistance by targeting GBP1. Furthermore, circ_0058608 could regulate GBP1 expression by sponging miR-1299. Circ_0058608 promoted the progression and taxol resistance of NSCLC by regulating the miR-1299/GBP1 axis.