Summary Chondrosarcomas are malignant cartilage tumours. They are poorly responsive to chemotherapy and radiotherapy. Treatment is usually limited to surgical resection; however, survival of patients with high‐grade chondrosarcoma is poor, even with wide surgical resection. Induction of apoptosis in chondrosarcoma cells, either directly or by enhancement of the response to chemotherapeutic drugs and radiation, may be a route by which outcome can be improved. In this article, we review potential molecular targets that regulate chondrocyte apoptosis and discuss the experimental evidence for their utility.

CSPG4/NG2 is a multifunctional transmembrane protein with limited distribution in adult tissues including articular cartilage. The purpose of this study was to investigate the possible roles of CSPG4/NG2 in chondrosarcomas and to establish whether this molecule may have potential for targeted therapy. Stable knock-down of CSPG4/NG2 in the JJ012 chondrosarcoma cell line by shRNA resulted in decreased cell proliferation and migration as well as a decrease in gene expression of the MMP (matrix metalloproteinase) 3 protease and ADAMTS4 (aggrecanase). Chondrosarcoma cells in which CSPG4/NG2 was knocked down were more sensitive to doxorubicin than wild-type cells. The results indicate that CSPG4/NG2 has roles in regulating chondrosarcoma cell function in relation to growth, spread and resistance to chemotherapy and that anti-CSPG4/NG2 therapies may have potential in the treatment of surgically unresectable chondrosarcoma.

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Sost mRNA suggesting that Sclerostin might be regulated by Wnt. We further observed an enhanced expression of Sclerostin in osteoarthritic cartilage compared to cartilage of control mice. Conclusions: We here show that Wnt3a increases the catabolic activity and inhibits the anabolic activity in murine chondrocytes. Sclerostin alleviates the expression of catabolic genes induced by Wnt and rescued proteoglycan production. Moreover, Sclerostin promotes the cartilage maintenance through the inhibition of chondrocyte hypertrophy. Finally, the expression of Sclerostin expression in osteoarthritic mice suggests that Sclerostin might be involved in the pathophysiology in cartilage damage and might constitute a target for the prevention of osteoarthritis.