MiR-503-5p functions as an oncogene in oral squamous cell carcinoma by targeting Smad7

Yifan Fei*, Weilan Shan* and Xiaoqing Chen

Department of Stomatology, Shanghai Changzheng Hospital, the Second Military Medical University, Shanghai, P.R. China
*These authors contributed equally to this work and should be considered as co-first authors

Offprint requests to: Xiaoqing Chen, Department of Stomatology, Shanghai Changzheng Hospital, the Second Military Medical University, 415 Fengyang Road, Shanghai 200003, P.R. China. e-mail: chen_xiaoqing479@126.com

Summary. Background. Oral squamous cell carcinoma (OSCC) is a common oral malignancy. Previous studies indicated that the level of miR-503-5p was upregulated in OSCC tissues. However, the mechanism by which miR-503-5p regulates the proliferation and invasion of OSCC cells remains unclear. Therefore, this study aimed to investigate the role of miR-503-5p during the progression of OSCC. Methods. The level of miR-503-5p in Tca8113 cells was detected using RT-qPCR assay. In addition, CCK-8, transwell assays and flow cytometry assays were conducted to detect cell viability, migration, invasion and apoptosis, respectively. Meanwhile, the dual luciferase reporter assay was applied to explore the interaction between miR-503-5p and Smad7 in Tca8113 cells. Results. Overexpression of miR-503-5p significantly promoted the proliferation, migration and invasion of Tca8113 cells, while downregulation of miR-503-5p markedly inhibited proliferation, migration and invasion of cells. In addition, knockdown of miR-503-5p obviously induced the apoptosis of Tca8113 cells via increasing the levels of Bax and cleaved caspase 3, and decreased the expression of Bcl-2. Moreover, SMAD family member 7 (Smad7) was identified as a direct binding target of miR-503-5p in Tca8113 cells. Overexpression of miR-503-5p significantly downregulated the levels of Smad7 and E-cadherin, but upregulated the levels of N-cadherin and MMP-9 in Tca8113 cells. Conclusion. These results indicated that miR-503-5p might act as an oncogene in OSCC cells by targeting Smad7. Therefore, miR-503-5p might act as a novel and potential therapeutic target for the treatment of OSCC. Histol Histopathol 35, 893-901 (2020)

Key words: Oral squamous cell carcinoma, miR-503-5p, Oncogene, Smad7, Apoptosis

DOI: 10.14670/HH-18-220