Interplay between receptor tyrosine kinases and hypoxia signaling in cancer |
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| Affiliation: | 1. Department of Radiation Oncology, Inselspital, Bern University Hospital, and University of Bern, 3010 Bern, Switzerland;2. Department of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3010 Bern, Switzerland;1. Studienpraxis Urologie, Nuertingen, Germany;2. Eberhard-Karls University Medical School, Tuebingen, Germany;3. Department of Urology, Albert-Ludwigs University, Freiburg, Germany;1. Laboratory of Genetic Disease and Perinatal Medicine and Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu 610041, Sichuan, PR China;2. Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu 610041, Sichuan, PR China;3. Division of Peptides Related with Human Disease, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, PR China;4. Department of Biochemistry and Molecular Biology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan, PR China;1. Hôpital Saint-Louis, université Paris 7 Paris Diderot, AP–HP, 75010 Paris, France;2. Hôpital Ambroise-Paré, université Versailles Saint-Quentin-en-Yvelines, AP–HP, 92100 Boulogne-Billancourt, France;3. Laboratoire des agents infectieux et hygiène, université de Saint-Étienne, CHU de Saint-Étienne, 42270 Saint-Étienne, France;4. LABOCEA R&D, CNRS, 29280 Plouzané, France;1. DITEP (Département d’Innovations Thérapeutiques et Essais Précoces), Gustave Roussy Cancer Campus, Villejuif, France;2. Faculté de médicine Paris-Sud XI, Kremlin-Bicêtre, France;3. U981 INSERM, Gustave Roussy Cancer Campus, Villejuif, France;4. Radiologie interventionnelle, Gustave Roussy Cancer Campus, Villejuif, France;5. Département de Médecine Oncologique, Gustave Roussy Cancer Campus, Villejuif, France;6. Laboratoire de Recherche Translationnelle et Centre de Ressources Biologiques, AMMICA, INSERM US23/CNRS UMS3655, Gustave Roussy Cancer Campus, Villejuif, France;7. Département de Biologie et Pathologie Médicales, Gustave Roussy Cancer Campus, Villejuif, France;8. Direction de la recherche clinique, Gustave Roussy Cancer Campus, Villejuif, France;1. Department of Obstetrics and Gynecology, University of Tennessee Health Science Center, Memphis, Tennessee;2. Department of Pathology, University of Tennessee Health Science Center, Memphis, Tennessee;3. Department of Obstetrics and Gynecology, Georgia Regents University, Augusta, Georgia;4. Department of Obstetrics and Gynecology, Wayne State University, Detroit, Michigan;1. University of Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, UMR9020 - UMR-S 1277 - Canther - Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France;2. Pathology Department, CHU Lille, University of Lille, Lille, France;3. Department of Biochemistry and Molecular Biology, Hormonology Metabolism Nutrition Oncology, CHU Lille, University of Lille, Lille, France;4. INSERM U-1018, CESP, Team 5 (EpReC, Renal and Cardiovascular Epidemiology), UVSQ, Villejuif, France;5. Thoracic Oncology Department, CHU Lille, University of Lille, Lille, France |
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| Abstract: | Deregulated signaling via receptor tyrosine kinase (RTK) pathways is prevalent in numerous types of human cancers and is commonly correlated with worst prognosis, resistance to various treatment modalities and increased mortality. Likewise, hypoxic tumors are often manifested by aggressive mode of growth and progression following an adaptive genetic reprogramming with consequent transcriptional activation of genes encoding proteins, which support tumor survival under low oxygen-related conditions. Consequently, both the hypoxia-inducible factor (HIF) system, which is the major mediator of hypoxia-related signaling, and numerous RTK systems are considered critical molecular targets in current cancer therapy. It is now evident that there is an intricate molecular crosstalk between RTKs and hypoxia-related signaling in the sense that hypoxia can activate expression of particular RTKs and/or their corresponding ligands, while some RTK systems have been shown to trigger activation of the HIF machinery. Moreover, signaling regulation of some RTK systems under hypoxic conditions has also been documented to take place in a HIF-independent manner. With this review we aim at overviewing the most current observations on that topic and highlight the importance of the potential co-drugging the HIF system along with particular relevant RTKs for better tumor growth control. |
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| Keywords: | RTKs Hypoxia HIF system Cancer VEGF |
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