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. Author manuscript; available in PMC: 2010 Feb 15.
Published in final edited form as: Cancer Res. 2009 Jan 27;69(4):1685–1692. doi: 10.1158/0008-5472.CAN-08-2164

Figure 6. The destructive cascade of prostate cancer derived PTHrP and its downstream action on CCL2 bone resorption and angiogenesis in skeletal lesions.

Figure 6

Prostate tumor cells release PTHrP, which stimulates CCL2 expression from osteoblasts. CCL2 causes increased osteoclastic bone resorption to facilitate prostate cancer tumor growth in bone. Meanwhile, CCL2 binds to its receptor on prostate tumor cells and stimulates the pro-angiogenic factor VEGF-A release from tumor cells. VEGF-A can further support tumor growth with enhanced neo-blood vessel formation. Thus, CCL2 plays a key role in the destructive cascade which favors tumor growth via activation of tumor cells, bone resorption and angiogenesis.