Abstract
Telomerase activation has very important implications for head and neck squamous cell carcinoma (HNSCC), but the regulatory mechanisms of telomerase in HNSCC remain unclear. In our present study, we found that miR-512-5P was markedly downregulated in telomerase-positive HNSCC cell lines. Both in vitro and in vivo assays revealed that miR-512-5P mimic attenuated HNSCC cell proliferation, and tumor growth in nude mice, which exerts its tumor suppressor function through elevated apoptosis, inhibition of the telomerase activity, decrease of telomere-binding proteins and shortening of telomere length by human telomerase reverse transcriptase (hTERT) downregulation. Furthermore, the dual-luciferase reporter gene assay results demonstrated that hTERT was a direct target of miR-512-5P. We conclude that the frequently miR-512-5P overexpression can regulate hTERT and function as a tumor suppressor in HNSCC. Therefore, miR-512-5P may serve as a potential therapeutic agent for miR-based HNSCC therapy.
Highlights
Head and neck squamous cell carcinoma (HNSCC) describes a broad range of various carcinomas including orbits, nasopharynx, oropharynx, oral cavity, hypopharynx, and larynx[1]
These findings suggested that miR-512-5p was reduced in telomerase positive HNSCC cell lines
Telomerase activity, which is essential for the maintenance of tumor cell immortality, is required for the survival of the majority of tumor cells probably critical for sustained tumor proliferation[16]
Summary
Head and neck squamous cell carcinoma (HNSCC) describes a broad range of various carcinomas including orbits, nasopharynx, oropharynx, oral cavity, hypopharynx, and larynx[1]. The incidence of HNSCC exceeds half a million annually, making it the fifth most common cancer diagnosed every year, which is a definitely important contributor to cancer related deaths[1]. In the past 20 years, despite recent marked progresses in diagnose and treatment of HNSCC, such as surgery, radiotherapy or chemotherapy, almost 30–50% of patients will undergo regional recurrence and distant metastases after the comprehensive treatments [2]. Searching for basic science research and development of novel therapeutic agents for HNSCC is significant and exciting.
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