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Int. J. Mol. Sci. 2017, 18(2), 383; doi:10.3390/ijms18020383

Splice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy

Team RNA Splicing, Cell Signaling and Response to Therapies, Institute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, University Grenoble Alpes, Grenoble 38702, France
These authors contribute equally to this work.
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Author to whom correspondence should be addressed.
Academic Editor: Akila Mayeda
Received: 12 December 2016 / Revised: 24 January 2017 / Accepted: 30 January 2017 / Published: 11 February 2017
(This article belongs to the Special Issue Pre-mRNA Splicing 2016)
View Full-Text   |   Download PDF [1506 KB, uploaded 11 February 2017]   |  

Abstract

Receptor tyrosine kinases (RTKs) belong to a family of transmembrane receptors that display tyrosine kinase activity and trigger the activation of downstream signalling pathways mainly involved in cell proliferation and survival. RTK amplification or somatic mutations leading to their constitutive activation and oncogenic properties have been reported in various tumour types. Numerous RTK-targeted therapies have been developed to counteract this hyperactivation. Alternative splicing of pre-mRNA has recently emerged as an important contributor to cancer development and tumour maintenance. Interestingly, RTKs are alternatively spliced. However, the biological functions of RTK splice variants, as well as the upstream signals that control their expression in tumours, remain to be understood. More importantly, it remains to be determined whether, and how, these splicing events may affect the response of tumour cells to RTK-targeted therapies, and inversely, whether these therapies may impact these splicing events. In this review, we will discuss the role of alternative splicing of RTKs in tumour progression and response to therapies, with a special focus on two major RTKs that control proliferation, survival, and angiogenesis, namely, epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor-1 (VEGFR1). View Full-Text
Keywords: alternative splicing; angiogenesis; cancer; EGFR; receptor tyrosine kinases; tumourigenesis; targeted therapies; VEGFR alternative splicing; angiogenesis; cancer; EGFR; receptor tyrosine kinases; tumourigenesis; targeted therapies; VEGFR
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Abou-Fayçal, C.; Hatat, A.-S.; Gazzeri, S.; Eymin, B. Splice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy. Int. J. Mol. Sci. 2017, 18, 383.

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