摘要
Multiple myeloma is characterized by the accumulation of malignant plasma cells in thebone marrow. Significant progress in molecular mechanisms of signaling pathways underlying the survival and/or proliferation of these cells has been achieved. Interleukin 6 （IL-6） is an important cytokine leading to multiple myeloma （MM） cells growth and survival. However, some MM cells isolated from MM patients are poorly responsive to IL-6 stimulation or IL-6 independent. This phenomenon raises the possibility that other growth factors may also be involved in the development of MM. Insulin like growth factor-I （IGF-I） plays an important role in the proliferation of a variety of cell types, in the development and growth of multiple tumors and in the prevention of apoptosis. IGF-I has recently been reported to play such a role in stimulating the MM cells growth, it even induces MM cells proliferation in IL-6 dependent cells, yet the detailed signaling components triggered by IGF-I have not been completely clarified. Thus, the present study are to address the signaling cascades triggered by IGF-I in MM cells.
Multiple myeloma is characterized by the accumulation of malignant plasma cells in thebone marrow. Significant progress in molecular mechanisms of signaling pathways underlying the survival and/or proliferation of these cells has been achieved. Interleukin 6 （IL-6） is an important cytokine leading to multiple myeloma （MM） cells growth and survival. However, some MM cells isolated from MM patients are poorly responsive to IL-6 stimulation or IL-6 independent. This phenomenon raises the possibility that other growth factors may also be involved in the development of MM. Insulin like growth factor-I （IGF-I） plays an important role in the proliferation of a variety of cell types, in the development and growth of multiple tumors and in the prevention of apoptosis. IGF-I has recently been reported to play such a role in stimulating the MM cells growth, it even induces MM cells proliferation in IL-6 dependent cells, yet the detailed signaling components triggered by IGF-I have not been completely clarified. Thus, the present study are to address the signaling cascades triggered by IGF-I in MM cells.
