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• W1566263874 abstract "// Ibtissem Djaafri 1,2,* , Farah Khayati 1,2,3,* , Suzanne Menashi 4 , Jorg Tost 5,6 , Marie-Pierre Podgorniak 3 , Aurelie Sadoux 1,3 , Antoine Daunay 6 , Luis Teixeira 7 , Jean Soulier 2,8 , Ahmed Idbaih 9,10 , Niclas Setterblad 1,2 , Françoise Fauvel 1,2 , Fabien Calvo 1,2 , Anne Janin 2,11,12 , Celeste Lebbé 2,13,14  and Samia Mourah 1,2 1 Inserm UMR-S 940 Paris, France 2 Institute of Hematology (IUH), U niversité Paris-Diderot, Sorbonne Paris Cité, Paris, France  3 AP-HP, Hôpital Saint-Louis, Laboratoire de Pharmacologie-Génétique, Paris, France  4 Université Paris Est Créteil, CNRS-UMR; Créteil, France 5 Laboratory for Epigenetics, Centre National de Génotypage, CEA-Institut de Génomique, Evry, France  6 Laboratory for Functional Genomics, Fondation Jean Dausset - CEPH, Paris, France  7 AP-HP ; Hôpital Saint-Louis, Service d’oncologie médicale, Paris, France 8 Hematology Laboratory APHP, Saint-Louis Hospital, Paris, France 9 AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Service de Neurologie 2-Mazarin, Paris, France 10 Inserm U 975, Paris, 75013 France, CNRS, UMR, Paris, France 11 Inserm, U728, Paris, France  12 AP-HP, Hôpital Saint-Louis, Laboratoire de Pathologie, Paris, France  13 AP-HP, Hôpital Saint-Louis, Département de Dermatologie, Paris, France  14 Inserm U976, Paris, France  * These Authors contributed equally to this work Correspondence: Samia Mourah, email: // Keywords : Tumor suppressor gene, Kindlin-3, Invasion/Migration, metastasis, Integrins Received : May 26, 2014 Accepted : June 18, 2014 Published : June 20, 2014 Abstract Kindlin-3 (FERMT-3) is known to be central in hemostasis and thrombosis control and its deficiency disrupts platelet aggregation and causes Leukocyte Adhesion Deficiency disease. Here we report that Kindlin-3 has a tumor suppressive role in solid cancer. Our present genetic and functional data show that Kindlin-3 is downregulated in several solid tumors by a mechanism involving gene hypermethylation and deletions. In vivo experiments demonstrated that Kindlin-3 knockdown in 2 tumor cell models (breast cancer and melanoma) markedly increases metastasis formation, in accord with the in vitro increase of tumor cell malignant properties. The metastatic phenotype was supported by a mechanism involving alteration in β3-integrin activation including decreased phosphorylation, interaction with talin and the internalization of its active form leading to less cell attachment and more migration/invasion. These data uncover a novel and unexpected tumor suppressor role of Kindin-3 which can influence integrins targeted therapies development." @default.
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• W1566263874 date "2014-06-18" @default.
• W1566263874 modified "2023-10-17" @default.
• W1566263874 title "A novel tumor suppressor function of Kindlin-3 in solid cancer" @default.
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• W1566263874 doi "https://doi.org/10.18632/oncotarget.2125" @default.
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