INTRODUCTIONHead and neck squamous cell carcinoma (HNSCC) is the sixth most prevalent malignancy worldwide. The induction of HNSCC has been ascribed to the abuse of tobacco, alcohol, and areca, to human papillomavirus infection, and to exposure to a number of other carcinogenic substances. The 5‐year survival rate for HNSCC remains low and, therefore, it has become important to explore in detail the molecular alterations that contribute to the development of HNSCC, both from the point of identifying tumor markers, and with the aim of improving choices in terms of therapeutic regimens.MicroRNAs (miRNAs) are noncoding RNAs that downregulate the expression of targeted genes by binding to the specific sequences in the 3′untranslated region (UTR) of the transcript via seed sequences. Many miRNAs are involved in the neoplastic process associated with HNSCC. Our previous studies have shown that there is drastic upregulation of miR‐31 in HNSCC. This upregulation can be evoked by activation of the epidermal growth factor receptor‐AKT‐CEBP/ß signaling cascade. Furthermore, miR‐31 enhances HNSCC oncogenicity by targeting FIH, Ku80, and ARID1A, which activates the hypoxia pathway, impairs gene repair, and enhances stemness properties. Additional oncogenic miRNAs also co‐target FIH together with miR‐31. The presence of salivary/serological miR‐31 has been validated
Head & Neck: Journal for the Sciences & Specialties of the Head and Neck – Wiley
Published: Jan 1, 2018
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