Mir-55 inhibition can reduce cell proliferation and induce apoptosis in Jurkat (Acute T cell Leukemia) cell line.

BACKGROUND: MicroRNAs are small and non-coding RNA molecules with approximately 22 nt in length that cause inhibition of translation or degradation of mRNA. MiR-155 is a kind of molecule with different functions, such as its role in proliferation, apoptosis, inflammation, differentiation, and immunity. One of its best known functions is apoptosis that affects on caspase-3 activity. The main aim of this study was evaluation of miR-155 inhibition effect on cell proliferation and apoptosis induction in Jurkat cells. MATERIAL AND METHODS: In this study, Jurkat cells along with MTT assay were used for evaluation of sensitivity to varied concentrations of miR-155 inhibitor (25, 50 and 75 nmol). MiR-155 expression level was analyzed using the quantitative real-time polymerase chain reaction (QRT-PCR). Caspase-3 activity was measured by caspase-3 colorimetric activity assay kit. Unpaired t-test was applied for the analysis of MTT and apoptosis results. Probability of 5% was assumed as statistically significant. RESULTS: According to our results, the use of miR-155 inhibitor increased the activity of caspase-3 by 2 fold in 75 nmol concentration. In this research, we found that the proper increase of miR-155 inhibitor concentration can inhibit miR-155 and consequently increase caspase-3 activity and induce apoptosis in the Jurkat cells leading to cell death ultimately. CONCLUSIONS: Apoptosis induction by miRNAs activation or inhibition is probably one of the best and low risk ways of cell death induction in malignancies. Due to role of miR-155 in several cancer cells, it may be used as a therapeutic target in future.

Lasting effects of early olfactory deprivation on the growth, DNA, RNA and protein content, and Na-K-ATPase and AchE activity of the rat olfactory bulb.

It is shown that when one of the olfactory bulbs (OB) of the rat is deprived of olfactory stimulation from birth, as compared to the normal OB on the opposite side, significant and permanent reductions in its growth and in several biochemical parameters take place as follows: weight gain, 25%; total DNA, 20--30%; total RNA, 30%; total protein, 30%; total Na-K-ATPase activity, 50%; total AChE activity, 20%. The concentrations of DNA, RNA and protein and the specific activity of AChE were not significantly affected but the specific activity of Na-K-ATPase was significantly reduced. In general, these interbulbar differences were seen in every experimental animal and were not due to hypertrophy or hyperplasia of the normal OB. These results suggest that olfactory stimulation during the early postnatal period has a significant influence on cell proliferation and cell growth as well as on the proliferation of neuronal membranes and synapses in the developing OB. It appears that the effects of olfactory deprivation are exerted during the first few weeks after birth when the bulb shows its most rapid period of growth and development, since (with the exception of DNA) the magnitude of the interbulbar difference did not increase appreciably by prolongation of olfactory deprivation beyond the early period. Thus in the rat the existence of a critical period encompassing the second and third postnatal weeks is suggested during which the developing OB appears to be especially vulnerable to the absence of olfactory stimulation.