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NOV (CCN3) regulation in the growth plate and CCN family member expression in cartilage neoplasia
Author(s) -
Yu Chunying,
Le AnhThy,
Yeger Herman,
Perbal Bernard,
Alman Benjamin A
Publication year - 2003
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1468
Subject(s) - cartilage , chondrocyte , ctgf , biology , cellular differentiation , pathology , microbiology and biotechnology , cancer research , medicine , growth factor , anatomy , genetics , gene , receptor
Growth plate chondrocytes undergo a coordinated differentiation process resulting in terminal differentiation and new bone formation. Enchondromas are pre‐malignant, benign cartilaginous lesions that arise from growth plate chondrocytes that fail to undergo terminal differentiation. NOV (nephroblastoma overexpressed) is a member of the CCN family of proteins, which share a common multi‐modular organization. While the role of NOV in chondrocyte development and cartilage neoplasia is not known, other CCN family members play a role in chondrocyte differentiation, or are differentially regulated in cartilage neoplasia. In embryonic murine growth plates, NOV was expressed in pre‐hypertrophic and early hypertrophic chondrocytes. PTHrP treatment (which inhibits terminal differentiation) decreased NOV expression in murine femurs maintained in organ culture, and decreased the activity of a NOV reporter construct in vitro . Expression of the CCN family members NOV, CTGF, CYR61, and WISP‐1 was examined in 15 chondrosarcomas of various grades and in three enchondromas. Expression of all of the family members was lower in the higher‐grade tumours. As identification of the grade of cartilage neoplasia can sometimes be difficult using histology alone, the level of expression of CCN family members could be a useful adjunct in the determination of tumour grade. Copyright © 2003 John Wiley & Sons, Ltd.