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To elucidate the regulatory effect of miRNA-1236-3p on the cellular behaviors of osteosarcoma (OS) cells, and to provide novel hallmarks and therapeutic targets for the diagnosis, treatment, and prognosis of OS.Relative level of miRNA-1236-3p in OS tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Regulatory effects of miRNA-1236-3p on the proliferative ability of HOS and U-2OS cells were evaluated by cell counting kit-8 (CCK-8) assay. Through flow cytometry, the potential influences of miRNA-1236-3p on cell cycle progression and apoptosis of OS cells were examined. Subsequently, the dual-luciferase reporter gene assay was conducted to explore the binding of KLF8 (Krüppel-like factor 8) to miRNA-1236-3p. Regulatory effects of KLF8 on cellular behaviors of OC cells were also evaluated.MiRNA-1236-3p was downregulated in OS tissues relative to controls. Meanwhile, miRNA-1236-3p was lowly expressed in OS with worse TNM stage or distant metastasis. The overexpression of miRNA-1236-3p in HOS and U-2OS cells suppressed the proliferative ability, arrested the cell cycle in the G0/G1 phase and induced apoptosis. Conversely, miRNA-1236-3p knockdown obtained the opposite trends. KLF8 was verified to bind to miRNA-1236-3p, and its expression was negatively regulated by miRNA-1236-3p in OS cells. A series of functional experiments displayed the oncogenic role of KLF8 in OS.MiRNA-1236-3p is downregulated in OS tissues and cell lines. The overexpression of miRNA-1236-3p suppresses the proliferative ability and induces apoptosis of OS cells via downregulating KLF8.

This study detected the expressions of microRNA-26a (miR-26a), miR-146a and miR-31 in lung tissues and BALF (bronchoalveolar lavage fluid) of asthma mice and children. Besides, cytokine levels of interleukin-5 (IL-5), IL-8, IL-12 and tumor necrosis factor-α (TNF-α) were detected as well. We aim to provide an experimental basis for clinical treatment of asthma.Forty female BALB/c mice were randomly assigned into control group and asthma group, respectively. Mice in asthma group (n=20) were immunized by intraperitoneal injection of OVA (ovalbumin) and provoked by atomization inhalation of OVA from the 15th day for 10 days. Mice in control group (n=20) were immunized and provoked with isodose saline during the same period. At the 26th day, mice were sacrificed for collecting lung tissues and BALF. Besides, we enrolled 17 cases of asthma children and 13 cases of children with airway foreign body as controls. BALF of each subject was collected. Total cellular score and differential counting in BALF were recorded. Expression levels of miR-26a, miR-146a, and miR-31 were detected by reverse transcription-polymerase chain reaction (RT-PCR). Levels of IL-5, IL-8, IL-12, and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA).The total cellular score in BALF of asthma mice and asthma children was higher than that of controls (p0.05). Percentages of eosinophils, neutrophils, and lymphocytes in BALF of asthma mice and asthma children were higher than those of controls, whereas the percentage of macrophages was lower (p0.05). Levels of IL-5, IL-8, IL-12, and TNF-α in lung tissues of asthma mice were markedly elevated compared with those of controls (p0.05). Similarly, levels of IL-5, IL-8, IL-12, and TNF-α were higher in BALF of asthma children than controls (p0.05). RT-PCR data showed higher mRNA levels of miR-26a, miR-146a, and miR-31 in lung tissues of asthma mice than controls (p0.05). The mRNA levels of miR-26a, miR-146a, and miR-31 in BALF of asthma children were highly expressed compared with those of controls as well (p0.05).MiR-26a, miR-146a, and miR-31 are involved in asthma progression mainly through regulating inflammatory factors and cells.