Targeting of miR‐31/96/182 to the Numb gene during head and neck oncogenesis

Targeting of miR‐31/96/182 to the Numb gene during head and neck oncogenesis 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Head & Neck: Journal for the Sciences & Specialties of the Head and Neck Wiley
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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
© 2018 Wiley Periodicals, Inc.
ISSN
1043-3074
eISSN
1097-0347
D.O.I.
10.1002/hed.25063
Publisher site
See Article on Publisher Site

Abstract

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

Journal

Head & Neck: Journal for the Sciences & Specialties of the Head and NeckWiley

Published: Jan 1, 2018

Keywords: ; ; ; ; ;

References

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