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MicroRNAs (miRNAs/miRs) are known to be involved in various human cancer types. Ultrasound-targeted microbubble destruction (UTMD) may improve the transfection efficiency of exogenous genes into target tissues and organs, thereby improving cancer treatment. In the present study, the role of miR-4284 in non-small cell lung cancer (NSCLC) was investigated and the effect of UTMD-mediated inhibition of miR-4284 on tumor progression was further analyzed. The expression of miR-4284 in NSCLC cells and tissues was detected by reverse transcription-quantitative PCR. UTMD-mediated inhibition of miR-4284 was achieved by co-transfection of microvesicles and miR-4284 inhibitors into NSCLC cells. A Cell Counting Kit-8 assay was used to determine NSCLC cell proliferation, and the migration and invasion of NSCLC cells were examined by Transwell assays. Compared with that in the control group, the expression of miR-4284 was increased in NSCLC tissues and cells. Knockdown of miR-4284 in NSCLC cells inhibited cell proliferation, migration and invasion. UTMD improved the transfection efficiency of miR-4284 inhibitors in NSCLC cells, resulting in more significant inhibition of tumor cell proliferation, migration and invasion. In conclusion, the results indicated that the expression of miR-4284 was increased in clinical samples and cell lines of NSCLC and that knockdown of miR-4284 inhibited the proliferation, migration and invasion of tumor cells. UTMD-mediated miR-4284 inhibition further promoted this effect, indicating that this technique may represent a novel strategy for the treatment of NSCLC. [ABSTRACT FROM AUTHOR]

Phosphoribosyl pyrophosphate synthetase 1 (PRPS1) is closely associated with a number of diseases; however, its influence in B-cell acute lymphoblastic leukemia (B-ALL) and the potential molecular mechanisms involved remain unclear. The present study aimed to evaluate the expression of PRPS1 in Chinese children with B-ALL and to investigate the mechanism of action of PRPS1 in this disease. A Cell Counting Kit-8 (CCK-8) assay was performed to examine the proliferation of B-ALL Sup-B15 and Raji cells, and flow cytometric analysis was conducted to determine the cell cycle distribution and rate of apoptosis. The mRNA and protein expression levels of PRPS1, MYC proto-oncogene, bHLH transcription factor, cyclin E1, B-cell lymphoma-2 (Bcl-2), cyclin dependent kinase 2 and caspase-3 were detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Elevated PRPS1 expression was associated with a high-risk stratification and poor prognosis in patients with B-ALL. Furthermore, overexpression of PRPS1 accelerated the growth of and inhibited apoptosis in Sup-B15 and Raji cells as well as increasing the expression of Bcl-2 to induce an anti-apoptotic effect in B-ALL cell lines. The results of the present study indicate that PRPS1 regulates multiple processes in B-ALL and may be an attractive therapeutic target. [ABSTRACT FROM AUTHOR]