Long Han1, Jian Cheng2, Afeng Li2. 1. Department of Stomatology, The Third Hospital Affiliated to Qiqihar Medical College, Qiqihar, China. 2. Department of Stomatology, The Shangluo Central Hospital, Shangluo, China.
Abstract
Background: Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. It was determined that circular RNAs were related to the development and progression of various cancers, including OSCC. The purpose of our study was to define the role and potential mechanism of hsa_circ_0072387 in OSCC progression. Materials and Methods: Thirty-five patients with OSCC were involved in this study. Real-time quantitative polymerase chain reaction was used to evaluate the expression levels of hsa_circ_0072387 and microRNA (miR)-503-5p. Cell proliferation, migration, and invasion abilities were assessed by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. The abundance of cell proliferation marker Ki-67, epithelial-mesenchymal transition (EMT) markers E-cadherin, N-cadherin, and vimentin was analyzed by Western blot assay. Glycolysis was evaluated using commercial kits. The interaction between hsa_circ_0072387 and miR-503-5p was confirmed by bioinformatics analysis, RNA immunoprecipitation (RIP) assay, and dual-luciferase reporter assay. Results: hsa_circ_0072387 expression was significantly downregulated, and miR-503-5p was upregulated in OSCC cells and tissues. Gain of hsa_circ_0072387 or knockdown of miR-503-5p suppressed the cell proliferation, migration and invasion, EMT, and glycolysis in OSCC SCC-4 and HSC-3 cells. hsa_circ_0072387 targeted miR-503-5p and inversely regulated miR-503-5p expression. Moreover, upregulation of miR-503-5p could partially revert the tumor-suppressive effects of hsa_circ_0072387 on OSCC cells. Conclusion: hsa_circ_0072387 inhibited OSCC progression by downregulating miR-503-5p, explicating that hsa_circ_0072387 could function as a novel potential therapeutic target for OSCC.
Background: Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. It was determined that circular RNAs were related to the development and progression of various cancers, including OSCC. The purpose of our study was to define the role and potential mechanism of hsa_circ_0072387 in OSCC progression. Materials and Methods: Thirty-five patients with OSCC were involved in this study. Real-time quantitative polymerase chain reaction was used to evaluate the expression levels of hsa_circ_0072387 and microRNA (miR)-503-5p. Cell proliferation, migration, and invasion abilities were assessed by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. The abundance of cell proliferation marker Ki-67, epithelial-mesenchymal transition (EMT) markers E-cadherin, N-cadherin, and vimentin was analyzed by Western blot assay. Glycolysis was evaluated using commercial kits. The interaction between hsa_circ_0072387 and miR-503-5p was confirmed by bioinformatics analysis, RNA immunoprecipitation (RIP) assay, and dual-luciferase reporter assay. Results: hsa_circ_0072387 expression was significantly downregulated, and miR-503-5p was upregulated in OSCC cells and tissues. Gain of hsa_circ_0072387 or knockdown of miR-503-5p suppressed the cell proliferation, migration and invasion, EMT, and glycolysis in OSCC SCC-4 and HSC-3 cells. hsa_circ_0072387 targeted miR-503-5p and inversely regulated miR-503-5p expression. Moreover, upregulation of miR-503-5p could partially revert the tumor-suppressive effects of hsa_circ_0072387 on OSCC cells. Conclusion: hsa_circ_0072387 inhibited OSCC progression by downregulating miR-503-5p, explicating that hsa_circ_0072387 could function as a novel potential therapeutic target for OSCC.