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Fig. 1 | Journal of Hematology & Oncology

Fig. 1

From: Role of protein kinases CK1α and CK2 in multiple myeloma: regulation of pivotal survival and stress-managing pathways

Fig. 1

CK1α or CK2 targeting determines MM plasma cell apoptosis through the deregulation of important MM survival signaling pathways. CK1α promotes β-catenin and AKT signaling while negatively control p53 in MM. Its inhibition (with D4476 or by RNAi) alone or in association with bortezomib or lenalidomide impinges on the activation of these survival events, promoting MM plasma cell death. CK2 sustains plasma cell survival and proliferation through the regulation of NF-κB, STAT3, and AKT. Its inactivation (with chemical compounds such as tBB, K27, CX-4945, or RNAi) alone or in association with old (melphalan) or new agents (bortezomib, Hsp90 inhibitors) causes plasma cell apoptosis and reduction in proliferation

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