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. Author manuscript; available in PMC: 2017 Jul 26.
Published in final edited form as: Mol Cancer Ther. 2011 Nov;10(11):2034–2042. doi: 10.1158/1535-7163.MCT-11-0433

Figure 3.

Figure 3

Bortezomib and deacetylase inhibitors (DACi) inhibit key pathways associated with multiple myeloma (MM) cell growth and survival. Growth and survival of MM cells are dependent on functioning intracellular pathways that drive proliferation of and the interaction with the extracellular matrix (ECM) and bone marrow stromal cells (BMSC). The combination of bortezomib and DACi leads to inactivation of NF-κB and MM cell apoptosis. Both DACi and bortezomib suppress the production of cytokines including interleukin-6 (IL-6) and insulin-like growth factor 1 (IGF1). Bortezomib also suppresses tumor necrosis factor α (TNF-α), leading to inhibition of the interaction of MM cells and BMSCs. Bortezomib has been shown to decrease the secretion of VEGF, leading to inhibition of angiogenesis. The cell surface proteoglycan syndecan 1 is downregulated by DACi, which affects the interaction of MM cells with the ECM. ICAM, intracellular adhesion molecule; LFA4, leukocyte function-associated antigen 4; STAT3, signal transducers and activators of transcription 3; VCAM, vascular cell adhesion molecule; VLA4, very late antigen 4.