C-myc expression is down-regulated in mafosfamide-treated HL-60 cells undergoing apoptosis
Related Experiment Video
Updated: Nov 7, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
1Department of Haematology, School of Pathology, University of the Witwatersrand, Parktown, South Africa.
Abstract:
The expression of the proto-oncogene c-myc has been strongly implicated in the regulation of apoptosis. Since we have previously shown apoptosis to occur in HL-60 leukemic cells exposed to the prodrug Mafosfamide (ASTA Z 7557), the present study was undertaken to examine the levels of c-myc mRNA transcripts in such cells. Mafosfamide, which is a cyclophosphamide derivative that rapidly generates 4-Hydroperoxycyclophosphamide after aqueous dissolution, was employed in doses ranging from 0.1 to 20 micrograms/ml. No changes in c-myc mRNA levels were evident after 1 hour of exposure to Mafosfamide. After 6 and 24 hours of Mafosfamide-exposure, however, there was a dose- and time-dependent decrease in c-myc transcripts. c-myc mRNA expression was reduced to a greater extent than was either beta-actin of GAPDH expression. Morphological, biochemical and ultrastructural evidence of apoptosis accompanied the Mafosfamide-induced c-myc mRNA down-regulation at 24 hours. We conclude that, in the context of Mafosfamide-treated HL-60 cells, upregulation of c-myc mRNA transcription was not fundamental for the activation of the apoptotic cascade.
Related Concept Videos
The Intrinsic Apoptotic Pathway
Abnormal Proliferation
Induced Pluripotent Stem Cells
Somatic cells are...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
MAPK Signaling Cascades
Cellular Injury V: Apoptosis and Autophagy