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

Warning

This publication doesn't include Faculty of Sports Studies. It includes Faculty of Science. Official publication website can be found on muni.cz.

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