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Objective: The aim of this study was to investigate long non-coding RNA (lncRNA) XIST expression in Wilms' tumor (WT) and to further explore its relationship with clinical features and prognosis of WT patients., Patients and Methods: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to examine the expression level of XIST in tumor tissue samples and paracancerous ones collected from 43 patients with renal cell carcinoma, and the interplay between XIST expression and clinical indicators, as well as prognosis of patients was analyzed. Meanwhile, XIST level in the nephroblast cancer cell line was further confirmed by qRT-PCR. In addition, XIST knockdown model was constructed using lentivirus in the WT cell lines, including HFWT and 17-94, and the influence of XIST on WT cell functions was analyzed through transwell assay. Finally, we investigated whether lncRNA XIST plays a role in the progression of WT by modulating microRNA-193a-5p., Results: In this research, qRT-PCR results revealed a significantly higher expression of lncRNA XIST in tumor tissue specimens of patients with renal cell carcinoma than that in adjacent ones. Compared with patients with low expression of lncRNA XIST, those with high XIST expression had a higher incidence of distant metastasis and a lower overall survival rate. Compared with the negative control group, the metastatic ability of WT cells in the lncRNA XIST knockdown group was markedly weakened. In addition, the results of qPCR showed that mRNA expression of lncRNA XIST and microRNA-193a-5p were negatively correlated in renal cell carcinoma tissue specimens. At the same time, silencing microRNA-193a-5p reversed the reduced metastasis ability of WT cells induced by knockdown of XIST., Conclusions: LncRNA XIST expression is dramatically enhanced in WT tissues and cell lines, which is closely associated with the incidence of distant metastasis and patients' poor prognosis. In addition, we demonstrated that lncRNA XIST may accelerate the malignant progression of WT via inhibiting microRNA-193a-5p.

Objective: To investigate the expression of microRNA-324-3p (miR-324-3p) in polycystic ovary syndrome (PCOS) and its effects on the proliferation and apoptosis of ovarian granulosa cells., Materials and Methods: A total of 60 Sprague-Dawley (SD) rats were randomly divided into normal group (n=30) and experimental group (n=30). Rats in the experimental group were intramuscularly injected with dehydroepiandrosterone (DHEA) (6 mg/100 g of body weight) and 0.2 mL oil for injection, while those in normal group were intramuscularly injected with 0.2 mL oil for injection. The ovarian tissues of PCOS model rats were removed to extract the total ribose nucleic acid (RNA). The expression of miR-324-3p was detected via reverse transcription-polymerase chain reaction (RT-PCR). Primary ovarian granulosa cells were isolated and cultured, and NC-miRNA and miR-324-3p mimic were transfected into cells. After 48 h, cell proliferation and apoptosis were detected via cell counting kit 8 (CCK-8) and flow cytometry assay, respectively. The targeted molecule of miR-324-3p was explored using bioinformatics, and dual-luciferase assay was performed to verify the effect of miR-324-3p on WNT2B expression. Granulosa cells were co-transfected with WNT2B-small-interfering RNA (siRNA) and miR-324-3p mimic, and then cell proliferation and apoptosis were detected via CCK-8 and flow cytometry assay, respectively., Results: The expression of miR-324-3p in ovarian tissues of PCOS group was significantly lower than that of normal group (p < 0.01). After transfection with miR-324-3p mimic into granulosa cells, cell proliferation was significantly inhibited and cell apoptosis was promoted (p < 0.01). MiR-324-3p exerted its effect on granulosa cells by directly targeting WNT2B. Silencing WNT2B expression could reverse the effects of miR-324-3p on proliferation and apoptosis of granulosa cells (p < 0.05)., Conclusions: The expression of miR-324-3p in the ovary of PCOS rats is decreased significantly. Overexpression of miR-324-3p can reduce the proliferation and induce the apoptosis of granulosa cells via targeting of WNT2B.

Objective: The current study was to explore the effect of melatonin on osteoporosis and relevant mechanisms., Materials and Methods: We performed micro-CT to detect bone microstructure and ELISA to detect the contents of osteocalcin (OCN) and bone alkaline phosphatase (BAP) in serum. Double fluorescence labeling of calcein and tetracycline and toluidine blue staining were used to determine morphological indexes of bone tissues. Alizarin red staining and Oil Red O staining were performed to recognize bone cells and adipocytes. RT-PCR was performed to determine the expression of osteoblast differentiation related genes., Results: In the current study, data from micro-CT indicated that melatonin significantly increased the bone mass density (BMD), bone volume/tissue volume (BV/TV), trabecular number (Tb.N) and trabecular thickness (Tb.Th), and decreased the Structure Model Index (SMI) and trabecular Separation/Spacing (Tb.Sp) in elderly rats. Melatonin reduced calcium and phosphorus losses in urine and increased BAP and OCN levels in serum in elderly rats and increased bone formation rate (BFR) and bone mineralization rate (MAR) in elderly rats. Melatonin increased the number of osteoblasts in bone marrow and reduced the number of adipocytes in elderly rats. Melatonin also promoted the expression of osteogenic differentiation genes and suppressed the expression of adipogenic differentiation genes., Conclusions: WE suggest that melatonin could alleviate osteoporosis in aged rats' models probably by promoting osteoblast differentiation.