Circ_0120175 promotes laryngeal squamous cell carcinoma development through up-regulating SLC7A11 by sponging miR-330-3p.

Abstract

The aim of our study was to illustrate the role of circular RNA 0120175 (circ_0120175) and its associated mechanism in laryngeal squamous cell carcinoma (LSCC) development. The abundance of circ_0120175, microRNA-330-3p (miR-330-3p) and solute carrier family 7, membrane 11 (SLC7A11) messenger RNA and protein was measured by quantitative real time polymerase chain reaction and Western blot assay. Cell proliferation, apoptosis, migration and invasion were assessed by cell counting kit-8 assay, flow cytometry and transwell migration and invasion assays, respectively. The interaction between miR-330-3p and circ_0120175 or SLC7A11 was confirmed by dual-luciferase reporter assay. Murine xenograft model was established to test the function of circ_0120175 in tumor growth in vivo. Circ_0120175 abundance was aberrantly increased in LSCC tissues and cell lines, and LSCC patients with high level of circ_0120175 were associated with advanced tumor staging, lymph node metastasis and short survival time. Circ_0120175 interference suppressed cell proliferation, migration and invasion and induced cell apoptosis of LSCC cells. Circ_0120175 could sponge and negatively regulate miR-330-3p expression in LSCC cells. The addition of anti-miR-330-3p partly reversed circ_0120175 knockdown-induced effects in LSCC cells. SLC7A11 bound to miR-330-3p. Circ_0120175 enhanced the abundance of SLC7A11 through sponging miR-330-3p in LSCC cells. Circ_0120175 silencing-mediated influences in LSCC cells were partly counteracted by the overexpression of SLC7A11. Circ_0120175 interference notably suppressed xenograft tumor growth in vivo. Circ_0120175 promoted proliferation, migration and invasion while impeded cell apoptosis of LSCC cells through miR-330-3p/SLC7A11 axis, which provided novel therapeutic targets for LSCC.