J Cancer 2020; 11(13):3871-3881. doi:10.7150/jca.43854 This issue Cite
1. Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, People's Republic of China.
2. Otolaryngology Major Disease Research Key Laboratory of Hunan Province, 87 Xiangya Road, Changsha, Hunan 410008, People's Republic of China.
3. Department of Hematology, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan 410008, People's Republic of China.
4. Department of Otolaryngology Head and Neck Surgery, Changsha Central Hospital,161 Shaoshan Road, University of South China, Changsha, Hunan 410004, People's Republic of China.
5. Department of Head and Neck Surgery, Hunan Cancer Hospital, The Affiliated Tumor Hospital of Xiangya Medical School, Central South University, 283 Tongzipo Road, Changsha, Hunan 410013, People's Republic of China.
6. Clinical Research Center for Pharyngolaryngeal Diseases and Voice Disorders in Hunan Province, 87 Xiangya Road, Changsha, Hunan 410008, People's Republic of China.
# These two authors contributed equally to this paper.
Invasion and metastasis represent the primary causes of therapeutic failure in patients diagnosed with squamous cell carcinoma of the head and neck (SCCHN). Therefore, disease prediction and inhibition of invasion and metastasis are critical for enhancing the survival of patients with SCCHN. Our previous study revealed that increased expression of miR-93-5p is associated with poor prognosis in SCCHN; however, the mechanism underlying the oncogenic functions of miR-93-5p in SCCHN migration and invasion remains unclear. Using qPCR analyses, transwell assays, and scratch tests, we demonstrated that expression of ectopic miR-93-5p induced the migration and invasion of SCCHN, and this was accompanied by corresponding alterations in biomarkers and transcription factors specific for epithelial-mesenchymal transition (EMT). Luciferase reporter assays were used to demonstrate that miR-93-5p directly targeted the 3' UTR of RGMB, and we further found that the tumor-promoting functions of miR-93-5p were partly mediated by targeting RGMB, whose downregulation also promoted the migration and invasion of SCCHN. Overall, our results indicate that miR-93-5p acts as an oncogene in the regulation of migration and invasion by suppressing RGMB in SCCHN. These findings provide novel evidence that miR-93-5p may serve as a valuable predictive biomarker and potential intervention target in patients with SCCHN.
Keywords: miR-93-5p, squamous cell carcinoma of the head and neck, RGMB, epithelial-mesenchymal transition