CircPVT1 facilitates the progression of oral squamous cell carcinoma by regulating miR-143-3p/SLC7A11 axis through MAPK signaling pathway.

Abstract

Oral squamous cell carcinoma (OSCC) is a common malignant tumor occurring in the oral cavity. Circular RNAs (circRNAs) play a crucial regulatory role in many cancers. This study aimed to investigate the function of circRNA plasmacytoma variant translocation 1 (PVT1) (circPVT1) in OSCC and its potential mechanism. The levels of circPVT1, solute carrier family 7 member 11 (SLC7A11), and microRNA-143-3p (miR-143-3p) were examined by quantitative real-time PCR (qRT-PCR) or western blot assay. Cell proliferation, apoptosis, migration, and invasion were evaluated by Cell Counting Kit-8 (CCK-8), colony formation assay, flow cytometry, and transwell assay. The levels of apoptosis and proliferation-related proteins were examined by western blot. The targeting relationship between miR-143-3p and circPVT1 or SLC7A11 was verified by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The levels of mitogen-activated protein kinase (MAPK) pathway-related proteins were measured by western blot. Xenograft assay was used to assess tumor growth in vivo. CircPVT1 and SLC7A11 were upregulated, while miR-143-3p was downregulated in OSCC tissues and cells. Silencing of circPVT1 or SLC7A11 suppressed proliferation, migration, and invasion and promoted apoptosis in OSCC cells. CircPVT1 upregulated SLC7A11 expression via sponging miR-143-3p. SLC7A11 upregulation alleviated the effect of circPVT1 knockdown on OSCC cell progression. Besides, circPVT1 modulated MAPK signaling pathway by regulating miR-143-3p. Moreover, circPVT1 knockdown inhibited tumor growth in vivo. Knockdown of circPVT1 impeded OSCC progression via the miR-143-3p/SLC7A11 axis through MAPK signaling pathway.