RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action
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Julien Masliah-Planchon1,2, Simon Garinet3 and Eric Pasmant3,4
1 Unité de Génétique Somatique, Département de Génétique Oncologique, Institut Curie, Paris, France
2 INSERM_U830, Institut Curie, Paris, France
3 Service de Biochimie et Génétique Moléculaire, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris, Paris, France
4 EA7331, Université Paris Descartes, Sorbonne Paris Cité, Faculté des Sciences Pharmaceutiques et Biologiques, Paris, France
Eric Pasmant, email:
Keywords: RAS MAPK pathway, microRNAs, cancer, epigenetics
Received: August 30, 2015 Accepted: November 22, 2015 Published: December 05, 2015
The highly conserved RAS-mitogen activated protein kinase (MAPK) signaling pathway is involved in a wide range of cellular processes including differentiation, proliferation, and survival. Somatic mutations in genes encoding RAS-MAPK components frequently occur in many tumors, making the RAS-MAPK a critical pathway in human cancer. Since the pioneering study reporting that let-7 miRNA acted as tumor suppressor by repressing the RAS oncogene, growing evidence has suggested the importance of miRNAs targeting the RAS-MAPK in oncogenesis. MiRNAs alterations in human cancers may act as a rheostat of the oncogenic RAS signal that is often amplified as cancers progress. However, specific mechanisms leading to miRNAs deregulation and their functional consequences in cancer are far from being fully elucidated. In this review, we provide an experimental-validated map of RAS-MAPK oncomiRs and tumor suppressor miRNAs from transmembrane receptor to downstream ERK proteins. MiRNAs could be further considered as potential genetic biomarkers for diagnosis, prognosis, or therapeutic purpose.
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