Yao Yao1, Xiao-Qin Liu1, Feng-Ying Yang2, Jing-Wen Mu2. 1. Department of Stomatology, Jingzhou Central Hospital, The Second Clinical Medical College, Yangtze University, Jingzhou, China. 2. Department of Stomatology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.
Abstract
OBJECTIVE: To explore the effect of miR-873-5p on proliferation, apoptosis, migration, and invasion of tongue squamous cell carcinoma (TSCC) by targeting SEC11A. METHODS: Tongue squamous cell carcinoma tissues were collected and performed by qRT-PCR and Western blotting to determine the expression of miR-873-5p and SPC18. SCC9 and CAL-27 cells were transfected and divided into Mock, mimic NC, miR-873-5p mimic, SEC11A, and miR-873-5p mimic + SEC11A groups. Then, a series of experiments including cell count kit 8 (CCK-8), wound healing, Transwell, and flow cytometry were conducted. Besides, Western blotting was used to detect the expression of SPC18 and EGFR pathway-related proteins. RESULTS: MiR-873-5p was downregulated while SPC18 was upregulated in TSCC, and miR-873-5p was negatively correlated with SPC18. Dual luciferase reporter gene assay confirmed SEC11A to be a target of miR-873-5p. Cell proliferation, migration, and invasion of SCC9 and CAL-27 cells in miR-873-5p mimic group were decreased with increased cell apoptosis, presenting with downregulations of SPC18 and EGFR pathway-related proteins, while cells in SEC11A group manifested totally different changes. Moreover, the inhibitory effect of miR-873-5p mimic on TSCC cell growth was abolished by SEC11A overexpression. CONCLUSION: Overexpression of miR-873-5p may suppress cell proliferation, migration, and invasion, but facilitate apoptosis in TSCC via targeting SEC11A.
OBJECTIVE: To explore the effect of miR-873-5p on proliferation, apoptosis, migration, and invasion of tongue squamous cell carcinoma (TSCC) by targeting SEC11A. METHODS: Tongue squamous cell carcinoma tissues were collected and performed by qRT-PCR and Western blotting to determine the expression of miR-873-5p and SPC18. SCC9 and CAL-27 cells were transfected and divided into Mock, mimic NC, miR-873-5p mimic, SEC11A, and miR-873-5p mimic + SEC11A groups. Then, a series of experiments including cell count kit 8 (CCK-8), wound healing, Transwell, and flow cytometry were conducted. Besides, Western blotting was used to detect the expression of SPC18 and EGFR pathway-related proteins. RESULTS: MiR-873-5p was downregulated while SPC18 was upregulated in TSCC, and miR-873-5p was negatively correlated with SPC18. Dual luciferase reporter gene assay confirmed SEC11A to be a target of miR-873-5p. Cell proliferation, migration, and invasion of SCC9 and CAL-27 cells in miR-873-5p mimic group were decreased with increased cell apoptosis, presenting with downregulations of SPC18 and EGFR pathway-related proteins, while cells in SEC11A group manifested totally different changes. Moreover, the inhibitory effect of miR-873-5p mimic on TSCC cell growth was abolished by SEC11A overexpression. CONCLUSION: Overexpression of miR-873-5p may suppress cell proliferation, migration, and invasion, but facilitate apoptosis in TSCC via targeting SEC11A.