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Published on: March 17, 2020
Circ_LPAR3 promotes the progression of oral squamous cell carcinoma (OSCC)
Li Li1, Ye Yin1, Fanglong Nan1
1Department of Stomatology, PLA 983rd Hospital, Tianjin, China.
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.
