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. 2011:2011:325238.
doi: 10.1155/2011/325238. Epub 2011 Feb 22.

Defective osteogenic differentiation in the development of osteosarcoma

Eric R Wagner  1 , Gaurav Luther, Gaohui Zhu, Qing Luo, Qiong Shi, Stephanie H Kim, Jian-Li Gao, Enyi Huang, Yanhong Gao, Ke Yang, Linyuan Wang, Chad Teven, Xiaoji Luo, Xing Liu, Mi Li, Ning Hu, Yuxi Su, Yang Bi, Bai-Cheng He, Ni Tang, Jinyong Luo, Liang Chen, Guowei Zuo, Richard Rames, Rex C Haydon, Hue H Luu, Tong-Chuan He
Affiliations

Defective osteogenic differentiation in the development of osteosarcoma

Eric R Wagner et al. Sarcoma. 2011.

V体育2025版 - Abstract

Osteosarcoma (OS) is associated with poor prognosis due to its high incidence of metastasis and chemoresistance. It often arises in areas of rapid bone growth in long bones during the adolescent growth spurt. Although certain genetic conditions and alterations increase the risk of developing OS, the molecular pathogenesis is poorly understood. Recently, defects in differentiation have been linked to cancers, as they are associated with high cell proliferation. Treatments overcoming these defects enable terminal differentiation and subsequent tumor inhibition. OS development may be associated with defects in osteogenic differentiation. While early regulators of osteogenesis are unable to bypass these defects, late osteogenic regulators, including Runx2 and Osterix, are able to overcome some of the defects and inhibit tumor propagation through promoting osteogenic differentiation VSports手机版. Further understanding of the relationship between defects in osteogenic differentiation and tumor development holds tremendous potential in treating OS. .

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V体育平台登录 - Figures

Figure 1
Figure 1
(a) Mesenchymal stem cells (MSCs) progress down the osteogenic differentiation cascade. MSCs are pluripotent bone marrow stromal cells that are able to differentiate into bone, muscle, tendon, and adipose tissue. Osteogenic differentiation of MSCs is a tightly regulated process by different signaling. Bone morphogenetic proteins (BMPs) and their downstream mediators, such as inhibitor of DNA binding (Id) proteins and connective tissue growth factor (CTGF), are early markers in the osteogenic differentiation cascade. Runx2 and Wnt proteins are important regulators of osteoblastic differentiation. Alkaline phosphatase and Osterix are early/middle markers, while osteocalcin and osteopontin are late markers of bone formation. (b) Defects in osteogenic differentiation lead to osteosarcoma (OS) development. If alterations in the MSC differentiation cascade block the progression to terminally differentiated osteoblasts or osteocytes, it is likely that tumorigenic precursors are formed. Such undifferentiated OS precursors would maintain the ability to proliferate and increase the risk for OS development. Although not well understood, some of the potential defects may include genetic and/or epigenetic changes in Wnt signaling, Rb, p53, and p27. These defects may lead to uncontrolled cell proliferation and disrupted differentiation. Thus, these alterations disrupt the delicate balance between proliferation and differentiation, leading to a tumorigenic phenotype.
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