Circular RNA circ_0067934 exhaustion expedites cell apoptosis and represses cell proliferation, migration and invasion in thyroid cancer via sponging miR-1304 and regulating CXCR1 expression.

Abstract

Distant metastasis or local recurrence is the leading cause of death in some patients with thyroid cancer (TC), a malignant tumor of the endocrine system. Circular RNA circ_0067934 (circ_0067934) has been reported to be connected with the tumorigenesis of multiple tumors. However, there are few reports on the role and regulatory mechanisms of circ_0067934 in TC. The expression levels of circ_0067934, protein kinase C iota (PRKCI), microRNA-1304 (miR-1304), and C-X-C chemokine receptor types 1 (CXCR1) were detected with quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The proliferation, apoptosis, migration, and invasion of TC cells were evaluated by Cell Counting Kit-8 (CCK8) assay, flow cytometry assay, and transwell assay, respectively. The relationship between circ_0067934 or CXCR1 and miR-1304 was confirmed with Dual-Luciferase reporter assay or RNA immunoprecipitation (RIP) assay. Protein level of CXCR1 was analyzed via Western blot analysis. Xenograft assay was executed to verify the role of circ_0067934 in vivo. Circ_0067934 and CXCR1 were enhanced and miR-1304 decreased in TC tissues and cells. Circ_0067934 downregulation triggered apoptosis and curbed proliferation, migration, and invasion of TC cells in vitro, as well as repressed tumor growth in vivo. Notably, circ_0067934 regulated CXCR1 expression via sponging miR-1304 in TC cells. Both miR-1304 silencing and CXCR1 elevation reversed the facilitation of apoptosis and the retardation of proliferation, migration, and invasion induced by circ_0067934 reduction in TC cells. Circ_0067934 downregulation expedited apoptosis and retarded proliferation, migration, and invasion of TC cells through miR-1304/CXCR1 axis.