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J. Teramachi et al.
Contributions
JT and MA designed the research and conceived the project; PCR was performed by JT, HT, AO and SS; flow cytometry by AO, MH and TH; immunoblotting by JT, HT, MH, AO, AB, TH, SN, MA, SS and MI; transfection by JT, HT, MH, AO and TH; and cell cultures by JT, HT, MH, AO, AB, TH, SN, MA, SS, MI, KS, MO, SF, KK and HM, JT, HT, MH, AO, TH, SN, MH, IE, TH, TM, and MA analyzed the data; JT and MA wrote the manuscript.
Funding
This work was supported in part by JSPS KAKENHI Grant Numbers JP18K08329, JP16K11504, JP17KK0169, JP18H06294; and Aki Horinouchi Research Grant; Japan Leukemia Research Fund; Yasuda Memorial Medical Foundation; the Ichiro Kanehara Foundation; and the Research Clusters program of Tokushima University. The funders had no role in study design, data collection and analysis, decision to pub- lish, or preparation of the manuscript.
References
1.Raje N, Roodman GD. Advances in the biology and treatment of bone disease in multiple myeloma. Clin Cancer Res. 2011; 17(6):1278-1286.
2.Silbermann R, Roodman GD. Myeloma bone disease: pathophysiology and man- agement. J Bone Oncol. 2013;2(2):59-69.
3. Tanaka Y, Abe M, Hiasa M, et al. Myeloma cell-osteoclast interaction enhances angio- genesis together with bone resorption: a role for vascular endothelial cell growth factor and osteopontin. Clin Cancer Res. 2007;13(3):816-823.
4.Cackowski FC, Anderson JL, Patrene KD, et al. Osteoclasts are important for bone angiogenesis. Blood. 2010;115(1):140-149.
5. Asano J, Nakano A, Oda A, et al. The ser- ine/threonine kinase Pim-2 is a novel anti- apoptotic mediator in myeloma cells. Leukemia. 2011;25(7):1182-1188.
6. Lu J, Zavorotinskaya T, Dai Y, et al. Pim2 is required for maintaining multiple myeloma cell growth through modulating TSC2 phosphorylation. Blood. 2013;122(9):1610- 1620.
7. Johrer K, Obkircher M, Neureiter D, et al. Antimyeloma activity of the sesquiterpene lactone cnicin: impact on Pim-2 kinase as a novel therapeutic target. J Mol Med (Berl). 2012;90(6):681-693.
8. Ehrlich LA, Chung HY, Ghobrial I, et al. IL- 3 is a potential inhibitor of osteoblast dif- ferentiation in multiple myeloma. Blood. 2005;106(4):1407-1414.
9.Giuliani N, Colla S, Morandi F, et al. Myeloma cells block RUNX2/CBFA1 activ- ity in human bone marrow osteoblast pro- genitors and inhibit osteoblast formation and differentiation. Blood. 2005; 106(7):2472-2483.
10.D'Souza S, del Prete D, Jin S, et al. Gfi1 expressed in bone marrow stromal cells is a novel osteoblast suppressor in patients with multiple myeloma bone disease. Blood. 2011;118(26):6871-6880.
11.Takeuchi K, Abe M, Hiasa M, et al. Tgf- Beta inhibition restores terminal osteoblast differentiation to suppress myeloma growth. PloS One. 2010;5(3):e9870.
12.Vallet S, Mukherjee S, Vaghela N, et al. Activin A promotes multiple myeloma- induced osteolysis and is a promising target for myeloma bone disease. Proc Natl Acad Sci U S A. 2010;107(11):5124-5129.
13. Hiasa M, Teramachi J, Oda A, et al. Pim-2 kinase is an important target of treatment for tumor progression and bone loss in myeloma. Leukemia. 2015;29(1):207-217.
14. Teramachi J, Hiasa M, Oda A, et al. Pim-2 is a critical target for treatment of osteoclas- togenesis enhanced in myeloma. Br J Haematol. 2018;180(4):581-585.
15.Mihaly SR, Ninomiya-Tsuji J, Morioka S. TAK1 control of cell death. Cell Death
Differ. 2014;21(11):1667-1676.
16. Sakurai H. Targeting of TAK1 in inflamma-
tory disorders and cancer. Trends
Pharmacol Sci. 2012;33(10):522-530. 17.Buglio D, Palakurthi S, Byth K, et al. Essential role of TAK1 in regulating mantle cell lymphoma survival. Blood. 2012;
120(2):347-355.
18. Safina A, Ren MQ, Vandette E, Bakin AV.
TAK1 is required for TGF-beta 1-mediated regulation of matrix metalloproteinase-9 and metastasis. Oncogene. 2008; 27(9):1198-1207.
19. Singh A, Sweeney MF, Yu M, et al. TAK1 inhibition promotes apoptosis in KRAS- dependent colon cancers. Cell. 2012; 148(4):639-650.
20. Tenshin H, Teramachi J, Oda A, et al. TAK1 inhibition subverts the osteoclastogenic action of TRAIL while potentiating its antimyeloma effects. Blood Adv. 2017; 1(24):2124-2137.
21. Wang LH, Yang XY, Zhang X, Farrar WL. Inhibition of adhesive interaction between multiple myeloma and bone marrow stro- mal cells by PPARgamma cross talk with NF-kappaB and C/EBP. Blood. 2007; 110(13):4373-4384.
22.Abe M, Hiura K, Ozaki S, Kido S, Matsumoto T. Vicious cycle between myeloma cell binding to bone marrow stro- mal cells via VLA-4-VCAM-1 adhesion and macrophage inflammatory protein-1alpha and MIP-1beta production. J Bone Miner Metab. 2009;27(1):16-23.
23. Zhu YX, Braggio E, Shi CX, et al. Identification of cereblon-binding proteins and relationship with response and survival after IMiDs in multiple myeloma. Blood. 2014;124(4):536-545.
24. Tang S, Ma D, Cheng B, et al. Crucial role of HO-1/IRF4-dependent apoptosis induced by panobinostat and lenalidomide in multiple myeloma. Exp Cell Res. 2018;363(2):196-207.
25.Fulciniti M, Amin S, Nanjappa P, et al. Significant biological role of sp1 transacti- vation in multiple myeloma. Clin Cancer Res. 2011;17(20):6500-6509.
26.Bat-Erdene A, Miki H, Oda A, et al. Synergistic targeting of Sp1, a critical tran- scription factor for myeloma cell growth and survival, by panobinostat and protea- some inhibitors. Oncotarget. 2016;7(48):79064-79075.
27.Kikuchi J, Wada T, Shimizu R, et al. Histone deacetylases are critical targets of bortezomib-induced cytotoxicity in multi- ple myeloma. Blood. 2010;116(3):406-417.
28. Yasui H, Hideshima T, Richardson PG, Anderson KC. Novel therapeutic strategies targeting growth factor signalling cascades in multiple myeloma. Br J Haematol. 2006; 132(4):385-397.
29. Damiano JS, Cress AE, Hazlehurst LA, Shtil AA, Dalton WS. Cell adhesion mediated
drug resistance (CAM-DR): role of integrins and resistance to apoptosis in human myeloma cell lines. Blood. 1999;93(5):1658- 1667.
30. Chauhan D, Uchiyama H, Akbarali Y, et al. Multiple myeloma cell adhesion-induced interleukin-6 expression in bone marrow stromal cells involves activation of NF- kappa B. Blood. 1996;87(3):1104-1112. Giuliani N, Colla S, Morandi F, Rizzoli V. The RANK/RANK ligand system is involved in interleukin-6 and interleukin-11 up-regulation by human myeloma cells in the bone marrow microenvironment. Haematologica. 2004;89(9):1118-1123.
32.Hiruma Y, Honjo T, Jelinek DF, et al. Increased signaling through p62 in the mar- row microenvironment increases myeloma cell growth and osteoclast formation. Blood. 2009;113(20):4894-4902.
33.Teramachi J, Silbermann R, Yang P, et al. Blocking the ZZ domain of sequesto- some1/p62 suppresses myeloma growth and osteoclast formation in vitro and induces dramatic bone formation in myelo- ma-bearing bones in vivo. Leukemia. 2016;30(2):390-398.
34. Mizukami J, Takaesu G, Akatsuka H, et al. Receptor activator of NF-kappaB ligand (RANKL) activates TAK1 mitogen-activat- ed protein kinase kinase kinase through a signaling complex containing RANK, TAB2, and TRAF6. Mol Cell Biol. 2002;22(4):992-1000.
35. Spinella-Jaegle S, Roman-Roman S, Faucheu C, et al. Opposite effects of bone morphogenetic protein-2 and transforming growth factor-beta1 on osteoblast differen- tiation. Bone. 2001;29(4):323-330.
36. Maeda S, Hayashi M, Komiya S, Imamura T, Miyazono K. Endogenous TGF-beta sig- naling suppresses maturation of osteoblas- tic mesenchymal cells. EMBO J. 2004;23(3):552-563.
37. Miyazono K. TGF-beta signaling by Smad proteins. Cytokine Growth Factor Rev. 2000;11(1-2):15-22.
38.Alliston T, Choy L, Ducy P, Karsenty G, Derynck R. TGF-beta-induced repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation. EMBO J. 2001;20(9):2254-2272.
39. Matsumoto T, Abe M. TGF-beta-related mechanisms of bone destruction in multi- ple myeloma. Bone. 2011;48(1):129-134.
40. Nyman JS, Merkel AR, Uppuganti S, et al. Combined treatment with a transforming growth factor beta inhibitor (1D11) and bortezomib improves bone architecture in a mouse model of myeloma-induced bone disease. Bone. 2016;91:81-91.
41. Lu A, Pallero MA, Lei W, et al. Inhibition of transforming growth factor-beta activation diminishes tumor progression and osteolyt- ic bone disease in mouse models of multi-
31.
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