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Purpose: To investigate the role of miR-598-3p in pediatric T-cell acute lymphoblastic leukemia (T- ALL). Methods: The expression of miR-598-3p in mononuclear cells isolated from the peripheral blood samples of children with or without T-ALL was assessed using real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Cell viability or proliferation of T-ALL cell lines was evaluated using cell counting kit-8 assay or bromodeoxyuridine staining, respectively. The target gene of miR-598-3p was predicted and validated using luciferase reporter assay, while the underlying mechanism involved in miR-598-3p-mediated T-ALL was determined by western blot analysis. Results: MiR-598-3p was reduced in the peripheral blood mononuclear cells of T-ALL patients. Ectopic miR-598-3p expression decreased T-ALL cell viability and suppressed proliferation, while miR-598-3p interference showed reversed effects. Additionally, the target gene of miR-598-3p, Dishevelled, EGL-10, and Pleckstrin domain-containing mTOR-interacting protein (DEPTOR), was down-regulated by miR- 598-3p in T-ALL. MiR-598-3p decreased phospho (p)-AKT protein expression, while AKT inhibition counteracted the suppressive effects of miR-598-3p silencing on T-ALL cell viability and proliferation. Conclusion: MiR-598-3p/DEPTOR is involved in the proliferation of T-ALL through AKT pathway, thus providing a potential novel application in pediatric T-ALL.

Background The genes in the PRR family are key components of the transcription-translation circadian network in plants, and comprise the core genes in the central oscillator translation feedback loop of Arabidopsis sp. They play important roles in several physiological processes and environmental adaptation. However, there is little information regarding the PRR genes of soybean, which is an important food crop. A genome-wide study of the PRR genes of soybean was performed herein using the available complete genome sequences of Glycine max and Glycine soja. Results In total, 12 PRR genes of G. max (GmPRR) and 14 PRR genes of G. soja (GsPRR) were identified and labelled according to their chromosomal location. The sequence length, relative molecular weight, and subcellular localization of the encoded proteins were predicted, and fundamental information was obtained for the genes. GmPRR and GsPRR were further categorized into three main groups based on their phylogenetic characteristics. The gene structures and characteristics of protein motifs were similar in the same subfamily. Conserved domain analyses of the proteins revealed that the integrity of the conserved domains differed among proteins from different subfamilies. GmPRR genes were absent on chromosomes 11 and 12, contrary to GsPRR genes. The results indicated that fragment replication events played an important role in the amplification of GmPRR and GsPRR genes. Intergenomic collinearity analysis of G. max, G. soja, and A. sp. revealed that the PRR genes of soybean and A. sp. were highly homologous. Analysis of transcriptome data revealed that the expression patterns of GmPRR genes differed at different times. Quantitative polymerase chain reaction (qPCR) analyses determined the relative transcript abundances of the different GmPRR and GsPRR varied across the studied plant materials. Conclusions In this study, 12 PRR genes of G. max (GmPRR) and 14 PRR genes of G. soja (GsPRR) were identified, and the structure, evolution, and expression patterns of the encoded proteins were investigated. The results of systematic analysis provides a basis for the subsequent identification of the functions of PRR genes, and the preliminary data can be used for analyzing the specific functions of the PRR genes of soybean.

Daidzein is a plant isoflavonoid primarily isolated from Pueraria lobate Radix as the dry root of P. lobata (Wild.) Ohwi, have long been used as nutraceutical and medicinal herb in China. Despite the report that daidzein can prevent neuronal damage and improve outcome in experimental stroke, the mechanisms of this neuroprotective action have been not fully elucidated. The aim of this study was to determine whether the daidzein elicits beneficial actions in a stroke model, namely, cerebral ischemia/reperfusion (I/R) injury, and to reveal the underlying neuroprotective mechanisms associated with the regulation of Akt/mTOR/BDNF signal pathway. The results showed that I/R, daidzein treatment significantly improved neurological deficits, infarct volume, and brain edema at 20 and 30 mg/kg, respectively. Meanwhile, it was found out that the pretreatment with daidzein at 20 and 30 mg/kg evidently improved striatal dopamine and its metabolite levels. In addition, daidzein treatment reduced the cleaved Caspase-3 level but enhanced the phosphorylation of Akt, BAD and mTOR. Moreover, daidzein at 30 mg/kg treatment enhanced the expression of BDNF and CREB significantly. This protective effect of daidzein was ameliorated by inhibiting the PI3K/Akt/mTOR signaling pathway using LY294002. To sum up, our results demonstrated that daidzein could protect animals against ischemic damage through the regulation of the Akt/mTOR/BDNF channel, and the present study may facilitate the therapeutic research of stroke.