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

• 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
• 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.

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