This study aimed to evaluate the effects of miR-93 on the growth and invasiveness of prostate cancer (PC) cells (PCCs). Real-time PCR was carried out to detect the expression of miR-93 in the PC tissues and cell lines. The adjacent normal tissues served as controls. For in vitro experiments, methyl thiazolyl tetrazolium, clone formation, tumor cell invasion assays, and western blot analysis (WBA) were performed to confirm the variations in the proliferation and invasiveness of PCCs, prior and subsequent to transfection with an miR-93 antisense oligonucleotide (ASO), which blocks miR-93 binding to its target. Furthermore, the effect of miR-93 on the proliferation of PCCs was examined. Finally, the expression levels of the target genes of miR-93 were determined by WBA. miR-93 expression was higher in PC tissues than in the adjacent normal tissues, and a reduction in the miR-93 level remarkably inhibited the proliferation and invasiveness of PCCs. Moreover, miR-93 enhanced the expression of its target genes TGFΒR2, ITGB8, and LATS2. The results of this study suggest that miR-93 may promote the proliferation and invasion of PCCs by upregulating its target genes TGFBR2, ITGB8, and LATS2.

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The mechanisms of hypertrophic cardiomyopathy (HCM) pathogenesis can be investigated by determining the differences between healthy and disease states at the molecular level. In the present study, large‑scale transcriptome sequencing was performed to compare mRNA expression in patients with HCM and control groups using an Illumina sequencing platform. Compared with the genome background, 257 differentially expressed genes (DEGs) were identified in which 62 genes were downregulated and 195 genes were upregulated. Reverse transcription‑quantitative polymerase chain reaction was performed to validate the expression pattern of certain mRNAs. Gene ontology enrichment and KEGG analysis of mRNAs was conducted to identify the biological modules and pathological pathways associated with the DEGs. To the best of our knowledge, this is the first time study to investigate the differences in mRNA between patients with HCM and normal controls at the transcriptome level. The results of the study will contributed to the understanding of the important molecular mechanisms involved in HCM and aid the selection of key genes to investigate in the future.

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The growth of microorganisms is often confined in restricting geometries. In this work, we designed a device to study the growth propagation of budding yeast along linear arrays of microfluidic chambers. Vacuum assisted cell loading was used to seed cells of limited numbers in the up-most chambers of each linear array. Once loaded, cells grow until confluent and then overgrow, pushing some of the newborns into the neighboring downstream chamber through connection channels. Such a scenario repeats sequentially along the whole linear chamber arrays. We observed that the propagation speed of yeast population along the linear arrays was strongly channel geometry dependent. When the connection channel is narrow and long, the amount of cells delivered into the downstream chamber is small so that cells grow over several generations in the same chamber before passing into the next chamber. Consequently, a population growth of more than 50 generations could be observed along a single linear array. We also provided a mathematical model to quantitatively interpret the observed growth dynamics.