It is still not known whether the GC induced upregulation of miR 223 affects GC induced apoptosis. Jones et al. showed that wide microRNA repression Ibrutinib 936563-96-1 happens during GCinduced apoptosis of rat thymocytes. is repression was associated with reduced expression of both nuclear and cytoplasmic microRNA processing enzymes. Silencing of Dicer in two human leukemic cell lines resulted in increased sensitivity to GC induced apoptosis. World wide downregulation of microRNA levels, especially the miR 17 family, by GCs was also seen in GC sensitive and painful ALL cell lines, with concomitant upregulation of Bim. Later studies showed that GCs selectively upregulate and downmodulate specic miRNAs that cannot be explained by altered Dicer expression. One polycistron chaos repressed by GCs is miR 1792, which regulates Bim term. Down-regulation of miR 1792 Endosymbiotic theory plays a part in the GC mediated upregulation of Bim. is microRNA chaos also represses PTEN, a negative regulator of the PI3K/Akt signaling pathway. Elizabeth GC mediated down-regulation of miR 1792 could be one mechanism responsible for the GC induced dephosphorylation of Akt. Key thymocytes based on mice transgenic for the miR 1792 polycistron people in the lymphocyte compartment displayed diminished sensitivity to GC induced apoptosis in lymphocytes, further supporting a role for GC induced repression of miR 1792 to advertise apoptosis. Harada et al. Noticed that GCs reduced miR 17 family expression in 500-watt of primary GC painful and sensitive ALL, but not in any of the GCresistant ones. Over-expression of miR 1792 attenuated GCinduced mobile death, while inhibition of miR 1792 improved the sensitivity to GC. ey also noted that in a pre B ALL cell line, a 10-hour dexamethasone treatment generated a lowering of miR 142 and miR 27a, while miR 9 was induced. ere is also some evidence that GCs may lower miR 27a expression in mouse muscle cells. Rainer et al. claimed an induction of the myeloid specic miR 223 CX-4945 structure and the cell cycle arrest and apoptosis inducing miR 1516 clusters by GC in a subset of T and T ALL cells, along with downregulation of the miR 1792 complex. A transient up-regulation of miR 181a and miR 19b was also observed. Overexpression of miR 15b16 mimics improved, whereas silencing by miR 15b16 inhibitors reduced GC awareness. Elizabeth miRNAs of the miR 1516 family are secured in two clusters embedded in the DLEU2 and SMC4 loci, respectively. ey have been implicated in arrest and in cell death/survival decisions, the latter apparently by targeting Bcl 2. Other microRNAs affected by GCs in pediatric ALL incorporate repression of miR 128b along side miR and upregulation of miR 548d 1 93, the paralogue of miR 1792.