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The aim of this study was to investigate the effects of long non-coding ribonucleic acid regulator of reprogramming (lncRNA ROR) on the proliferation and apoptosis of endometrial cancer (EC) cells, and to explore its possible underlying mechanism.The expression levels of lncRNA ROR and Notch1 in EC tissues were detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The changes in Notch1 protein were detected via Western blotting. Subsequently, the regulatory mechanism of lncRNA ROR on Notch1 was analyzed using Luciferase reporter gene assay. Moreover, the changes in cell proliferation and apoptosis were determined through cell counting kit-8 (CCK-8) assay and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, respectively.Both lncRNA ROR and Notch1 were highly expressed in EC tissues (p0.05). After overexpression of lncRNA ROR, HEC-1A cells had significantly enhanced proliferation (p0.05) and weakened apoptosis (p0.05). Meanwhile, the mRNA and protein levels of Notch1 rose remarkably compared with those in control group (p0.05). Luciferase reporter gene assay revealed that lncRNA ROR could bind to the Notch1 regulatory factor miR-34a and inhibit its activity.LncRNA ROR regulates the proliferation and apoptosis of EC cells via promoting the expression of Notch1 protein.

The aim of the current study was to investigate the potential roles of miR-215-3p in the progression of cervical cancer.The levels of miR-215-3p in both cervical cancer tissues and cell lines were detected using quantitative Real-time polymerase chain reaction (qRT-PCR) assay. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, migration and invasion assays were applied to investigate the role of miR-215-3p on the growth and aggressiveness of cervical carcinoma SiHa cell. The expression of SRY-Box 9 (SOX9) was assessed by Western blotting assay. The Xenograft model and lung metastasis model were applied to reveal the impact of miR-215-3p on the growth and distant metastasis of cervical carcinoma cell in vivo. Moreover, miR-215-3p and a SOX9 siRNA were co-transfected into the SiHa cell to investigate the underlying mechanism of miR-215-3p-SOX9 on cervical cancer tumorigenesis.We used genome-wide gene expression analysis using clinical cervical cancer samples to identify that miR-215-3p was down-regulated in cervical cancer. We then collected 31 pairs of cervical cancer and the corresponding non-cancerous tissues to determine miR-215-3p level and indicated that miR-215-3p was significantly down-expressed in cervical cancer. Furthermore, the functional analysis suggested that over-expression of miR-215-3p suppressed the aggressiveness of SiHa cell, whereas down-regulation led to the opposite results. We identified SOX9 as a direct target of miR-215-3p, and its level was negatively related to the level of miR-215-3p in cervical carcinoma tissue. Up-regulation of SOX9 reversed the suppressive impact of miR-215-3p on cervical carcinoma cell, and down-regulation of SOX9 reversed the promote effects of miR-215-3p CONCLUSIONS: These findings showed the important role of the miR-215-3p/SOX9 axis in the progression of cervical carcinoma.

To investigate the potential effect of miR-487b/IL-33-ST2 axis on the pathology of allergic rhinitis (AR) and the relevant mechanism.The expression level of interleukin-33 (IL-33), a homolog of sulfotransferase (ST2), and miR-487b were detected in patients with or without allergic rhinitis. Luciferase assay was performed to evaluate the interaction between miR-487b and IL-33, and the effects of miR-487b/IL-33-ST2 axis on allergic rhinitis mice were determined by established allergic rhinitis model in mice by ovalbumin (OVA). The levels of OVA-specific immunoglobulin E (Ig-E), proinflammatory cytokines (IL-4, IL-5, and IL-13), and pathological alterations were detected.The level of IL-33 and its specific ligand ST2 were found increased in allergic rhinitis patients while miR-487b expression level was markedly repressed. To confirm whether miR-487b has a regulation effect on IL-33, we checked it in three publicly available algorithms, TargetScan, miRDB, and microRNA. We found that IL-33 is a direct target of miR-487b, and Luciferase assays confirmed our hypothesis, the subsequent experiments showed that up-regulation of miR-487b could inhibit expression of IL-33 and ST2, resulting in the decrease of the immunoglobulin E (Ig-E), proinflammatory cytokines and mitigation of pathological alterations.Our research discovered the suppressor function of miR-487b in allergic rhinitis and revealed that miR-487b/IL-33-ST2 axis may be a potential therapeutic target for the treatment of allergic rhinitis.