Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE RESEARCH
DOI: 10.1038/s41598-018-36728-y
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Funding
- Institut National de la Recherche (INSERM)
- Centre National de la Recherche Scientifique (CNRS)
- University Grenoble Alpes
- Comite Departemental Isere de la Ligue Nationale contre le Cancer
- Institut National du Cancer [INCa-PLBIO 16-085]
- INCa/DHOS (Appel d'Offre Recherche Translationnelle)
- Fondation de France (Projet Grande Ampleur)
- ROCHE fellowship (Bourse de Recherche Fondamentale)
- Fondation ARC pour la Recherche Contre le Cancer
- Fonds de dotation AGIR pour les Maladies Chroniques
- Ligue Nationale Contre Le Cancer
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The splice variant sVEGFR1-i13 is a truncated version of the cell membrane-spanning VEGFR1 receptor that is devoid of its transmembrane and tyrosine kinase domains. We recently showed the contribution of sVEGFR1-i13 to the progression and the response of squamous lung carcinoma to anti-angiogenic therapies. In this study, we identify VEGF(165), a splice variant of VEGF-A, as a regulator of sVEGFR1-i13 expression in these tumors, and further show that VEGF(165) cooperates with the transcription factor SOX2 and the splicing factor SRSF2 to control sVEGFR1-i13 expression. We also demonstrate that anti-angiogenic therapies up-regulate sVEGFR1-i13 protein level in squamous lung carcinoma cells by a mechanism involving the VEGF(165)/SOX2/SRSF2 network. Collectively, our results identify for the first time a signaling network that controls VEGFR1 pre-mRNA alternative splicing in cancer cells.
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