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. Author manuscript; available in PMC: 2018 Mar 15.
Published in final edited form as: Cancer Res. 2017 Feb 15;77(6):1492–1502. doi: 10.1158/0008-5472.CAN-16-2755

Fig.7. Schematic illustration depicts the roles of Syk signaling in VEGF-D overexpression and TSC2-null tumor growth.

Fig.7

In TSC2-deficient cells, activation of mTORC1 and Syk signaling induces MCP-1 overproduction via a Stat3-dependent manner. Subsequently, MCP-1 recruits and activates peripheral blood mononuclear cells (PBMCs), leading to increased VEGF-D expression. In contrast, treatment with Syk inhibitors impairs proliferation of TSC2-deficient cells and decreases production of MCP-1. As a result, VEGF-D expression is reduced in PBMCs.