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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

c-Myc overcomes cell cycle inhibition by CBFbeta- SMMHC, a myeloid leukemia oncoprotein.

Thirty percent of acute myeloid leukemia cases express a Core Binding Factor ( CBF) oncoprotein or harbor point mutations in one or both AML1 (RUNX1) genes. Each of these alterations reduces endogenous CBF activities. CBFbeta- SMMHC is expressed from the inv(16) chromosome in 8% of AML cases and inhibits endogenous CBF DNA-binding. Inhibition of CBF reduces Retinoblastoma protein phosphorylation and slows the G(1) to S cell cycle transition. c-Myc, a protein which stimulates S phase entry, is over-expressed in one-third of AMLs. We have developed Ba/F3 cell lines in which zinc regulates CBFbeta- SMMHC expression and 4-hydroxytamoxifen activates c-Myc-ER. In these lines, c-Myc-ER overcomes inhibition of cell cycle progression mediated by CBFbeta- SMMHC. CBFbeta- SMMHC does not affect endogenous c-Myc RNA levels, indicating that CBF does not regulate the c-Myc gene. Conversely, c-Myc-ER does not alter CBF DNA-binding activity. Thus, c-Myc-ER acts downstream of CBFbeta- SMMHC to stimulate cell cycle progression. In a subset of CBF leukemias, elevated expression of c-Myc is expected to facilitate the proliferation of the leukemic blasts and thereby potentiate the ability of CBF oncoproteins to block differentiation.[1]

References

  1. c-Myc overcomes cell cycle inhibition by CBFbeta-SMMHC, a myeloid leukemia oncoprotein. Bernardin, F., Yang, Y., Civin, C.I., Friedman, A.D. Cancer Biol. Ther. (2002) [Pubmed]
 
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