Circ_LPAR3 promotes the progression of oral squamous cell carcinoma

Background: circ_LPAR3 is an oncogene in esophageal squamous cell carcinoma. However, its role in oral squamous cell carcinoma (OSCC) is unknown. Purpose: To reveal the functions of circ_LPAR3 in OSCC. Methods: Online bioinformatic analysis was performed to disclose the differential expression of circ_LPAR3, VEGFC, AKT1 in OSCC and also the target predictions of miR-513b-5p. Transfection was applied in OSCC cells. RT-qPCR was used to detect the RNA expression and western blot to measure the proteins, VEGFC and phosphor-AKT1 (ser473, p-AKT1). CCK8 kit was used for viability detection and Flow cytometry for apoptosis evaluation. RNA pull-down and luciferase reporter methods were used to validate the binding sites to miR-513b-5p on circ_LPAR3, VEGFC and AKT1. OSCC mice models were established to further unveil the functions of circ_LPAR3 in OSCC in vivo. H&E staining and immunohistochemistry (CD34, VEGFC and p-AKT1) were further applied to analyze the pathological changes in association with circ_LPAR3 downregulation. Results: circ_LPAR3 was upregulated in OSCC. Its knockdown in cells could decrease cell survival and mobility and in mice model, could inhibit the tumor growth and angiogenesis. Circ_LPAR3 promoted VEGFC and AKT1 activity by sponging miR-513b-5p in OSCC cells. Conclusion: Knockdown of circ_LPAR3 could inhibit the OSCC progression by sponging miR-513b-5p and activating VEGFC and AKT1.

Automated summary

circ_LPAR3 is upregulated in oral squamous cell carcinoma (OSCC), and its knockdown can inhibit tumor growth and angiogenesis by sponging miR-513b-5p and activating VEGFC and AKT1.