The microRNA miR-29c-5p inhibits cell proliferation and migration by targeting TMEM98 in head and neck carcinoma

• Published in: Aging (Albany, NY.) Vol. 13; no. 1; pp. 769 - 781
• Main Authors: Li, Jingjia, Chen, Weixiong, Luo, Lixia, Liao, Lieqiang, Deng, Xuequan, Wang, Yuejian
• Format: Journal Article
• Language: English
• Published: United States Impact Journals 15.01.2021
• Subjects: Animals; Apoptosis - genetics; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; G2 Phase Cell Cycle Checkpoints - genetics; Gene Expression Regulation, Neoplastic - genetics; Head and Neck Neoplasms - genetics; Humans; In Vitro Techniques; Membrane Proteins - genetics; Mice; MicroRNAs - genetics; Neoplasm Transplantation; Research Paper; Squamous Cell Carcinoma of Head and Neck - genetics; microRNA; TMEM98; proliferation; metastasis; head and neck squamous cell carcinoma
• ISSN: 1945-4589; 1945-4589
• DOI: 10.18632/aging.202183

Head and neck squamous cell carcinoma (HNSCC), which occurs frequently worldwide, is characterized by high risk of metastasis. MicroRNAs (miRNAs) play crucial roles in tumorigenesis and cancer development. In this study, miR-29c-5p was identified using three high throughput microarrays. We measure miR-29c-5p expression in HNSCC tissues and cell lines. To determine the function of miR-29c-5p in HNSCC, we evaluated its effects in vitro on cell proliferation, the cell cycle, apoptosis, and cell migration. We employed a mouse tumor xenograft model to determine the effects of miR-29c-5p on tumors generated by HNSCC cell lines. The miR-29c-5p expression was lower in HNSCC tissues than in normal tissues. Upregulated miR-29c-5p expression in HNSCC cells inhibited migration and arrested cells in the G2/M phase of the cell cycle. Further, upregulated miR-29c-5p expression inhibited the proliferation of HNSCC cells and . In addition, transmembrane protein 98 (TMEM98) was identified as a direct target of miR-29c-5p by using a luciferase reporter assay. These findings provide new insights that link the regulation of miR-29c-5p expression to the malignant phenotype of HNSCC and suggest that employing miR-29c-5p may serve as a therapeutic strategy for managing patients with HNSCC.