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Background: Curcumin is a natural chemical component that has an anticancer effect. The aim of this study was to explore the potential molecular mechanism of curcumin regulating lung cancer (LC) progression. Methods: The expression of circRUNX1, miR-760 and Ras-like GTPase 3D (RAB3D) was detected by qRT-PCR. Cell proliferation were determined by CCK8 assay and colony formation assay. Cell apoptosis, migration and invasion were detected by flow cytometry, wound healing and transwell assays. Protein levels were examined by western blot (WB) analysis. RNA interaction was confirmed by dual-luciferase reporter assay. LC xenograft tumors were constructed using BALB/c nude mice. Results: CircRUNX1 was upregulated in LC and its expression could be inhibited by curcumin. Curcumin reduced LC cell proliferation, metastasis, and accelerate apoptosis, while circRUNX1 overexpression reversed these effects. MiR-760 was confirmed to be a target of circRUNX1, which could reverse the effects of circRUNX1 on curcumin-treated LC cell functions. RAB3D was a target of miR-760, and its knockdown reversed the promotion effect of miR-760 inhibitor on the progression of curcumin-treated LC cells. Conclusion: Curcumin suppressed LC progression via circRUNX1/miR-760/RAB3D axis. [ABSTRACT FROM AUTHOR]

Background: Circular RNAs (circRNAs) have emerged as vital regulators in human cancers, including colorectal cancer (CRC). In this study, we aimed to explore the roles of circRUNX1 in CRC. Methods: The levels of circRUNX1, RUNX1 mRNA, solute carrier family 38 member 1 (SLC38A1) mRNA and microRNA‐485‐5p (miR‐485‐5p) were determined by quantitative real‐time polymerase chain reaction (qRT‐PCR) analysis. The protein level of SLC38A1 was measured by Western blot assay. Cell colony formation, migration, invasion and apoptosis were assessed by colony formation assay, wound‐healing assay, Transwell assay and flow cytometry analysis, respectively. The interaction between miR‐485‐5p and circRUNX1 or SLC38A1 was verified by dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The levels of extracellular glutamine, intracellular glutamate and α‐ketoglutarate (α‐KG) were measured with specific kits. The functional role of circRUNX1 in CRC development in vivo was explored by murine xenograft model assay. Results: CircRUNX1 was upregulated in CRC tissues and cells compared with normal tissues and cells. CircRUNX1 deficiency restrained CRC cell colony formation, migration, invasion and glutaminolysis and induced apoptosis in vitro as well as blocked tumour growth in vivo. CircRUNX1 directly sponged miR‐485‐5p, which negatively modulated SLC38A1 expression in CRC cells. The effects of circRUNX1 knockdown on CRC cell colony formation, migration, invasion, apoptosis and glutaminolysis were reversed by miR‐485‐5p inhibition. Moreover, miR‐485‐5p overexpression repressed the malignant behaviours of CRC cells, with SLC38A1 elevation overturned the impacts. Conclusion: CircRUNX1 promoted CRC cell growth, metastasis and glutamine metabolism and repressed apoptosis by elevating SLC38A1 through sponging miR‐485‐5p, which might provide a novel target for CRC treatment. [ABSTRACT FROM AUTHOR]