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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Mol Cancer Ther. 2011 Dec 1;11(2):267–276. doi: 10.1158/1535-7163.MCT-11-0584

Figure 1. Osteoblast-secreted FGF8f in the presence of RA regulates osteoblastic differentiation in an autocrine manner.

Figure 1

(A) Morphology of U2OS cells treated with RA or transduced with lentiviral RARαS77A or FGF8f. (B) WB analysis of FGF8f in the conditioned medium collected from U2OS cells treated with RA (left) or transduced by RARαS77A (middle) or FGF8f (right). (C) Proliferation analysis by cell count (left) and qRT-PCR depiction of OPN (right). *P<0.05. (D) Bone differentiation induced by RA stimuli or FGF8f overexpression, as judged by ARS staining (top), and FGF8 antibody neutralization of FGF8f-induced bone differentiation (bottom). Ab, antibodies.