Circ‐SATB2 (hsa_circ_0008928) and miR‐150‐5p are regulators of TRIM66 in the regulation of NSCLC cell growth and metastasis of NSCLC cells via the ceRNA pathway

Abstract

AbstractCircular RNA (circRNA) was an important modulator and potential molecular target of nonsmall cell lung cancer (NSCLC). CircSATB2 was reported to be upregulated in NSCLC. However, the role and mechanism of circSATB2 in NSCLC progression remain to be illustrated. The RNA and protein expression was detected by quantitative real‐time polymerase chain reaction, western blot, and immunohistochemistry assay. Cell counting kit‐8, cell colony formation, and 5‐ethynyl‐2′‐deoxyuridine assays were applied to assess cell growth. The migrated and invaded cells were examined by transwell assay. Flow cytometry was performed to measure apoptotic cells. The interaction among circSATB2, microRNA‐150‐5p (miR‐150‐5p), and tripartite motif‐containing protein 66 (TRIM66) was identified by dual‐luciferase reporter assay and RNA immunoprecipitation assay. An in vivo experiment was conducted to investigate the effect of circSATB2 on tumor growth. CircSATB2 expression was highly expressed in NSCLC tissues and cell lines. CircSATB2 and TRIM66 silencing both suppressed NSCLC cell growth, migration, and invasion whereas promoted NSCLC cell apoptosis. CircSATB2 acted as a molecular sponge for miR‐150‐5p, and miR‐150‐5p interacted with the 3′ untranslated region (3′UTR) of TRIM66. Moreover, circSATB2 knockdown‐induced effects were partly reversed by TRIM66 overexpression in NSCLC cells. Besides, cirSATB2 expression was negatively correlated with miR‐150‐5p level and positively correlated with TRIM66 level in NSCLC tumor tissues. CircSATB2 knockdown blocked xenograft tumor growth in vivo. In summary, this study verified that circSATB2 stimulated NSCLC cell malignant behaviors by miR‐150‐5p/TRIM66 pathway, providing a possible circRNA‐targeted therapy for NSCLC.