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

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Authors	KREJČÍ Pavel PROCHÁZKOVÁ Jiřina SMUTNÝ Jiří CHLEBOVÁ Katarína LIN Patricia AKLIAN Anie BRYJA Vítězslav KOZUBÍK Alois WILCOX William R.
Year of publication	2010
Type	Article in Periodical
Magazine / Source	Bone
MU Faculty or unit	Faculty of Science
Citation
Field	Genetics and molecular biology
Keywords	FGFR3; Oncogene; Skeletal dysplasia; Cartilage; MAP kinase; Senescence
Description	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.
Related projects:	Functional and molecular characteristics of cancer and normal stem cells - identification of targets for novel therapeutics and therapeutic strategies Novel pathway of FGFR3 signaling in achondroplasia