scholarly journals Inhibition of p38α Mitogen-Activated Protein Kinase Prevents the Development of Osteolytic Bone Disease, Reduces Tumor Burden, and Increases Survival in Murine Models of Multiple Myeloma

2007 ◽  
Vol 67 (10) ◽  
pp. 4572-4577 ◽  
Author(s):  
Karin Vanderkerken ◽  
Satya Medicherla ◽  
Les Coulton ◽  
Hendrik De Raeve ◽  
Angelo Willems ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Protein Kinase ◽  
Bone Disease ◽  
Tumor Burden ◽  
Mitogen Activated Protein Kinase ◽  
Murine Models ◽  
Osteolytic Bone Disease ◽  
Mitogen Activated Protein

scholarly journals Antitumor effect of dobutamine on multiple myeloma via mitogen-activated protein kinase  pathwayin vitro

2016 ◽  
Vol 48 (12) ◽  
pp. 1135-1137 ◽  
Author(s):  
Bingqian Xie ◽  
Zhijian Xu ◽  
Guang Yang ◽  
Gege Chen ◽  
Bo Li ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Protein Kinase ◽  
Antitumor Effect ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein

Macrophage inflammatory protein 1-alpha (MIP-1α) triggers migration and signaling cascades mediating survival and proliferation in multiple myeloma (MM) cells

Blood ◽  
2003 ◽  
Vol 101 (9) ◽  
pp. 3568-3573 ◽  
Author(s):  
Suzanne Lentzsch ◽  
Margarete Gries ◽  
Martin Janz ◽  
Ralf Bargou ◽  
Bernd Dörken ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Protein Kinase ◽  
Mapk Pathway ◽  
Bone Destruction ◽  
Mitogen Activated Protein Kinase ◽  
Bone Lesions ◽  
Inflammatory Protein ◽  
Mitogen Activated Protein ◽  
And Migration ◽  
Macrophage Inflammatory Protein

Recently, it has been demonstrated that macrophage inflammatory protein 1- alpha (MIP-1α) is crucially involved in the development of osteolytic bone lesions in multiple myeloma (MM). The current study was designed to determine the direct effects of MIP-1α on MM cells. Thus, we were able to demonstrate that MIP-1α acts as a potent growth, survival, and chemotactic factor in MM cells. MIP-1α–induced signaling involved activation of the AKT/protein kinase B (PKB) and the mitogen-activated protein kinase (MAPK) pathway. In addition, inhibition of AKT activation by phosphatidylinositol 3- kinase (PI3-K) inhibitors did not influence MAPK activation, suggesting that there is no cross talk between MIP-1α–dependent activation of the PI3-K/AKT and extracellular-regulated kinase (ERK) pathway. Our data suggest that besides its role in development of osteolytic bone destruction, MIP-1α also directly affects cell signaling pathways mediating growth, survival, and migration in MM cells and provide evidence that MIP-1α might play a pivotal role in the pathogenesis of MM.

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