Blood Res 2015; 50(2):
Published online June 25, 2015
https://doi.org/10.5045/br.2015.50.2.87
© The Korean Society of Hematology
1Department of Drug Activity, New Drug Development Center, Medical Innovation Foundation, Osong, Korea.
2Department of Internal Medicine, School of Medicine, Chungnam National University, Daejeon, Korea.
Correspondence to : Correspondence to Deog-Yeon Jo, M.D., Ph.D. Division of Hematology/Oncology, Department of Internal Medicine, Chungnam National University Hospital, 282, Munhwa-ro, Jung-gu, Daejeon 301-721, Korea. Tel: +82-42-280-7162, Fax: +82-42-257-5753, deogyeon@cnu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Bortezomib is widely used for the treatment of multiple myeloma. Bone marrow stromal cells (BMSCs) endow myeloma cells with survival and growth advantages. However, the influence of bortezomib on BMSCs is not well elucidated. We examined the effects of bortezomib on the survival and growth of BMSCs
The effects of bortezomib on the survival and proliferation of the BMSC MS-5 cell line and on BMSCs obtained from healthy individuals (N=4) and newly diagnosed myeloma patients (N=5) were investigated
Bortezomib inhibited BMSC proliferation in a concentration-dependent manner, and induced cellular apoptosis. Bortezomib decreased CXCL12 production by BMSCs. Knockdown of CXCL12 mRNA in BMSCs revealed that CXCL12 served as an autocrine growth factor. Short-term bortezomib treatment of BMSC monolayers reduced the tendency of myeloma cells to locate to positions under the monolayers.
Bortezomib inhibits the survival and growth of BMSCs
Keywords Bone marrow stromal cells, Bortezomib, CXCL12, Multiple myeloma, Proliferation, Survival
Blood Res 2015; 50(2): 87-96
Published online June 25, 2015 https://doi.org/10.5045/br.2015.50.2.87
Copyright © The Korean Society of Hematology.
Ha-Yon Kim1, Ji-Young Moon2, Haewon Ryu2, Yoon-Seok Choi2, Ik-Chan Song2, Hyo-Jin Lee2, Hwan-Jung Yun2, Samyong Kim2, and Deog-Yeon Jo2*
1Department of Drug Activity, New Drug Development Center, Medical Innovation Foundation, Osong, Korea.
2Department of Internal Medicine, School of Medicine, Chungnam National University, Daejeon, Korea.
Correspondence to: Correspondence to Deog-Yeon Jo, M.D., Ph.D. Division of Hematology/Oncology, Department of Internal Medicine, Chungnam National University Hospital, 282, Munhwa-ro, Jung-gu, Daejeon 301-721, Korea. Tel: +82-42-280-7162, Fax: +82-42-257-5753, deogyeon@cnu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Bortezomib is widely used for the treatment of multiple myeloma. Bone marrow stromal cells (BMSCs) endow myeloma cells with survival and growth advantages. However, the influence of bortezomib on BMSCs is not well elucidated. We examined the effects of bortezomib on the survival and growth of BMSCs
The effects of bortezomib on the survival and proliferation of the BMSC MS-5 cell line and on BMSCs obtained from healthy individuals (N=4) and newly diagnosed myeloma patients (N=5) were investigated
Bortezomib inhibited BMSC proliferation in a concentration-dependent manner, and induced cellular apoptosis. Bortezomib decreased CXCL12 production by BMSCs. Knockdown of CXCL12 mRNA in BMSCs revealed that CXCL12 served as an autocrine growth factor. Short-term bortezomib treatment of BMSC monolayers reduced the tendency of myeloma cells to locate to positions under the monolayers.
Bortezomib inhibits the survival and growth of BMSCs
Keywords: Bone marrow stromal cells, Bortezomib, CXCL12, Multiple myeloma, Proliferation, Survival
Bortezomib inhibits the proliferation of bone marrow stromal cells (BMSCs). MS-5 cells
Bortezomib induces delayed apoptosis of bone marrow stromal cells (BMSCs). Cells were incubated in appropriate growth media, without or with bortezomib (5-500 nM), for 24-72 hr. Apoptosis was measured by flow cytometry after staining the cells for annexin V.
Knockdown of chemokine (CXC motif) ligand 12 (CXCL12) inhibits the spontaneous proliferation of bone marrow stromal cells (BMSCs). BMSCs from 3 normal individuals
Bortezomib downregulates the expression and production of chemokine (CXC motif) ligand 12 (CXCL12) in MS-5 cells. MS-5 cells were incubated without or with bortezomib (5-500 nM) in X-VIVO medium for 24 hr prior to reverse transcription-PCR
Bortezomib downregulates the expression and production of chemokine (CXC motif) ligand 12 (CXCL12) in bone marrow stromal cells (BMSCs). BMSCs from 3 normal individuals
Bortezomib and dexamethasone exert an additive downregulation of chemokine (CXC motif) ligand 12 (CXCL12) levels in MS-5 cells.
Fatıma Ceren Tuncel, Istemi Serin, Sacide Pehlivan, Yasemin Oyaci, Mustafa Pehlivan
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Blood Res 2013; 48(1): 35-39Se Ryeon Lee, Seok Jin Kim, Yong Park, Hwa Jung Sung, Chul Won Choi, and Byung Soo Kim
Korean J Hematol 2010; 45(3): 183-187
Bortezomib inhibits the proliferation of bone marrow stromal cells (BMSCs). MS-5 cells
Bortezomib induces delayed apoptosis of bone marrow stromal cells (BMSCs). Cells were incubated in appropriate growth media, without or with bortezomib (5-500 nM), for 24-72 hr. Apoptosis was measured by flow cytometry after staining the cells for annexin V.
Knockdown of chemokine (CXC motif) ligand 12 (CXCL12) inhibits the spontaneous proliferation of bone marrow stromal cells (BMSCs). BMSCs from 3 normal individuals
Bortezomib downregulates the expression and production of chemokine (CXC motif) ligand 12 (CXCL12) in MS-5 cells. MS-5 cells were incubated without or with bortezomib (5-500 nM) in X-VIVO medium for 24 hr prior to reverse transcription-PCR
Bortezomib downregulates the expression and production of chemokine (CXC motif) ligand 12 (CXCL12) in bone marrow stromal cells (BMSCs). BMSCs from 3 normal individuals
Bortezomib and dexamethasone exert an additive downregulation of chemokine (CXC motif) ligand 12 (CXCL12) levels in MS-5 cells.