{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(19)"],"submitter":["Djaafri I"],"pubmed_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 tal"],"journal":["Oncotarget"],"pagination":["8970-85"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4253411"],"repository":["biostudies-literature"],"pubmed_title":["A novel tumor suppressor function of Kindlin-3 in solid cancer."],"pmcid":["PMC4253411"],"pubmed_authors":["Daunay A","Soulier J","Sadoux A","Teixeira L","Lebbe C","Khayati F","Fauvel F","Setterblad N","Tost J","Janin A","Mourah S","Idbaih A","Podgorniak MP","Menashi S","Calvo F","Djaafri I"],"additional_accession":[]},"is_claimable":false,"name":"A novel tumor suppressor function of Kindlin-3 in solid cancer.","description":"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 tal","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Oct","modification":"2025-04-22T20:38:44.992Z","creation":"2019-03-27T01:40:47Z"},"accession":"S-EPMC4253411","cross_references":{"pubmed":["25344860"],"doi":["10.18632/oncotarget.2125"]}}