Because both oleic acid and palmitic acid are reported to stimulate adipocytic differentiation [ 43], we speculate that they potentiate the negative effect of EGF and FGF2 on the expression of activation markers by enforcing the transdifferentiation of human aHSCs towards the more adipogenic qHSC phenotype.
We tested this in myeloid-committed granulo-monocytic progenitors (GMPs) by enforcing Ddit3 expression, resulting in a transient re-acquisition of self-renewal potential and a dramatic change in the nature of the colonies obtained, with the predominance of large GM colonies of immature appearance.
In their in vitro experiments carried out on APL blasts, Valleron et al. noticed that transcription of these snoRNAs was lost under all-trans retinoic acid-mediated differentiation and induced by enforced expression of the PML RARalpha fusion protein in negative leukemic cell lines.
If so, differentiation should be blocked by enforced Nanog expression.
In a number of studies, p21 has actually been reported to protect tumor cells against cell death induced by enforced p53 expression [ 26] or by low doses of cytotoxic agents [ 13, 27- 30].
This is supported by the rescue of the senescence phenotype by enforced expression of C/EBPβ.
Relative to the in vitro generation of EpiSC, reprogramming by enforced expression can provide complementary information on the role of TFs in promoting acquisition of pluripotency.
We used single-cell gene expression profiling of GMPs, either wild-type or transduced with a control vector or a Ddit3-expressing lentivirus, to interrogate the transcriptional program changes imposed by enforced expression of Ddit3 and to inspect its role in remodeling of the transcriptional networks underlying lineage progression and/or identity.
At the molecular level the development of cervical cancer is driven by enforced expression of two oncoproteins (E6 and E7) encoded by the HR-HPV types [ 6].
Furthermore, enforced expression of B-RAFV600E in melanocytes resulted in decreases in the BimS mRNA and protein, but intriguingly, the levels of the BimL mRNA and protein were increased by enforced expression of B-RAFV600E These results suggest that regulation of Bim splicing by mutant B-RAF is more complex than inhibition of splicing of BimS, and may vary between different cell types.
