International Journal of Hematology and Oncology
2024, Vol 34, Num 4 Page(s): 189-198
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Differentiation Inducing Factor-1 Represses c-Myc and VEGF Expression in Myeloma Cells
Rajni KUMARI1, Rehan KHAN1, Alpana SHARMA1
All India Institute of Medical Sciences, Department of Biochemistry, New Delhi, INDIA
Keywords: c-Myc, VEGF, DIF-1, Multiple myeloma, RPMI8226
Cell adhesion mediated-drug resistance (CAM-DR) is designated as the culprit of relapsed and refractory multiple myeloma (MM). c-Myc and VEGF overexpression in MM is correlated with MM progression and CAM-DR in bone marrow microenvironment. c-Myc is responsible for hyperproliferation of myeloma cells whereas VEGF induces angiogenesis to support the hyperproliferation. Hence, c-Myc and VEGF represent the promiscuous targets in MM. In this study, we have examined online databases to verify the severity of c-Myc and VEGF expression in MM. Effect of differentiation inducing factor-1 (DIF-1) was studied by treating RPMI8226 cells with DIF-1 (10 μM) followed by qRT-PCR, western blotting, and cell proliferation by XTT. DIF-1 targets c-Myc and VEGF expression at both transcriptional and translational level in RPMI8226 cells. DIF-1 activates GSK-3β, which may influence c-Myc and VEGF expression. Hence, DIF-1 inhibits cell proliferation of MM cells. Our report is a maiden attempt to reveal that DIF-1 could act as an adjunct drug to overcome chemoresistance in MM in future.
Rajni KUMARI1, Rehan KHAN1, Alpana SHARMA1
All India Institute of Medical Sciences, Department of Biochemistry, New Delhi, INDIA
Keywords: c-Myc, VEGF, DIF-1, Multiple myeloma, RPMI8226
Cell adhesion mediated-drug resistance (CAM-DR) is designated as the culprit of relapsed and refractory multiple myeloma (MM). c-Myc and VEGF overexpression in MM is correlated with MM progression and CAM-DR in bone marrow microenvironment. c-Myc is responsible for hyperproliferation of myeloma cells whereas VEGF induces angiogenesis to support the hyperproliferation. Hence, c-Myc and VEGF represent the promiscuous targets in MM. In this study, we have examined online databases to verify the severity of c-Myc and VEGF expression in MM. Effect of differentiation inducing factor-1 (DIF-1) was studied by treating RPMI8226 cells with DIF-1 (10 μM) followed by qRT-PCR, western blotting, and cell proliferation by XTT. DIF-1 targets c-Myc and VEGF expression at both transcriptional and translational level in RPMI8226 cells. DIF-1 activates GSK-3β, which may influence c-Myc and VEGF expression. Hence, DIF-1 inhibits cell proliferation of MM cells. Our report is a maiden attempt to reveal that DIF-1 could act as an adjunct drug to overcome chemoresistance in MM in future.
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