Expression of hsa-MIR-204, RUNX2, PPARγ, and BCL2 in Bone Marrow Derived Mesenchymal Stem Cells from Multiple Myeloma Patients and Normal Individuals

Document Type : Original Article


1 Department of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

2 Department of Hematology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran

3 Bone Marrow Transplantation Center, Taleghani Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran

4 Department of Clinical Biochemistry, Faculty of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Iran


Objective: Multiple Myeloma (MM) is a heterogeneous cytogenetic disorder in which clonal plasma cells proliferate in the bone marrow (BM) and cause bone destruction. The BM microenvironment plays a crucial role in pathogenesis of this disease, and mesenchymal stem cells (MSCs) are one of the key players. Herein, we propose to investigate the expressions of hsa-MIR-204, runt-related transcription factor 2 (RUNX2), peroxisome proliferator-activated receptor gamma (PPARγ), and B-cell lymphoma 2 (BCL2) as factors involved in osteogenesis, adipogenesis, and MSC survival in BM-MSCs from MM patients and normal individuals.
Materials and Methods: In this experimental study, we isolated MSCs from BM aspirates of MM patients and healthy donors. Total RNA were extracted before and after co-culture with L363 myeloma cells. Gene expressions of RUNX2, PPARγ, BCL2, and hsa-MIR-204 were assessed by quantitive real time polymerase chain reaction (qRT-PCR).
Results: Higher levels of RUNX2, PPARγ, and hsa-MIR-204 expressions existed in MMMSCs compared to normally derived (ND)-MSCs. BCL2 expression decreased in MMMSCs. We observed different results in the co-culture model.
Conclusion: In general, the MM-MSCs gene expression profile differed compared to NDMSCs. Upregulation of RUNX2, PPARγ, and hsa-MIR-204 in MM-MSCs compared to NDMSCs would result in formation of bone defects. Downregulation of BCL2 would lead to MM-MSC cell death.