FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence

KREJČÍ, Pavel, Jiřina PROCHÁZKOVÁ, Jiří SMUTNÝ, Katarína CHLEBOVÁ, Patricia LIN, Anie AKLIAN, Vítězslav BRYJA, Alois KOZUBÍK and William R. WILCOX. FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence. Bone. USA: Elsevier Science, 2010, neuveden, No 47, p. 102-110. ISSN 8756-3282.

Basic information

• Original name: FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence
• Authors: KREJČÍ, Pavel (203 Czech Republic, guarantor, belonging to the institution), Jiřina PROCHÁZKOVÁ (203 Czech Republic, belonging to the institution), Jiří SMUTNÝ (203 Czech Republic, belonging to the institution), Katarína CHLEBOVÁ (703 Slovakia, belonging to the institution), Patricia LIN (840 United States of America), Anie AKLIAN (840 United States of America), Vítězslav BRYJA (203 Czech Republic, belonging to the institution), Alois KOZUBÍK (203 Czech Republic, belonging to the institution) and William R. WILCOX (840 United States of America).
• Edition: Bone, USA, Elsevier Science, 2010, 8756-3282.

Other information

• Original language: English
• Type of outcome: Article in a journal
• Field of Study: Genetics and molecular biology
• Country of publisher: United States of America
• Confidentiality degree: is not subject to a state or trade secret
• Impact factor: Impact factor: 4.601
• RIV identification code: RIV/00216224:14310/10:00044238
• Organization unit: Faculty of Science
• UT WoS: 000279150400012
• Keywords in English: FGFR3; Oncogene; Skeletal dysplasia; Cartilage; MAP kinase; Senescence

Abstract

FGFR3 signaling is capable of inducing premature senescence in chondrocytes, manifested as reversible, ERK-dependent growth arrest accompanied by alteration of cellular shape, loss of the extracellular matrix, upregulation of senescence markers (alpha-GLUCOSIDASE, FIBRONECTIN, CAVEOLIN 1, LAMIN A, SM22alpha and TIMP 1), and induction of senescence-associated beta-GALACTOSIDASE activity. Our data support a model whereby FGFR3 signaling inhibits cartilage growth via exploiting cellular response originally designed to eliminate cells harboring activated oncogenes.

Links

• GA301/09/0587, research and development project: Name: Nové dráhy FGFR3 signalingu v achondroplázii

Investor: Czech Science Foundation, Novel pathway of FGFR3 signaling in achondroplasia

• MSM0021622430, plan (intention): Name: Funkční a molekulární charakteristiky nádorových a normálních kmenových buněk - identifikace cílů pro nová terapeutika a terapeutické strategie

Investor: Ministry of Education, Youth and Sports of the CR, Functional and molecular characteristics of cancer and normal stem cells - identification of targets for novel therapeutics and therapeutic strategies