Journal
MOLECULAR CANCER RESEARCH
Volume 5, Issue 10, Pages 1053-1062Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-07-0145
Keywords
-
Categories
Funding
- NCI NIH HHS [P30 CA013330, 2P30CA13330] Funding Source: Medline
- NHLBI NIH HHS [1F32 HL077242-0102, R01 HL078381, HL78381] Funding Source: Medline
Ask authors/readers for more resources
Malignant transformation often leads to both loss of normal proliferation control and inhibition of cell differentiation. Some tumor cells can be stimulated to reenter their differentiation program and to undergo terminal growth arrest. The in vitro differentiation of mouse erythroleukemia (MEL) cells is an important example of tumor cell reprogramming. MEL cells are malignant erythroblasts that are blocked from differentiating into mature RBC due to dysregulated expression of the transcription factor PU.1, which binds to and represses GATA-1, the major transcriptional regulator of erythropolesis. We used RNA interference to ask whether inhibiting PU.1 synthesis was sufficient to cause MEL cells to lose their malignant properties. We report here that transfection of MEL cells with a PU.1-specific short interfering RNA oligonucleotide causes the cells to resume erythroid differentiation, accumulate hemoglobin, and undergo terminal growth arrest. RNA interference directed at specific, aberrantly expressed transcription factors may hold promise for the development of potent antitumor therapies in other hematologic malignancies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available