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Background: Since the optimal surgery for isolated medial knee osteoarthritis (OA) is unclear, this study aimed at comparing the effectiveness of unicondylar knee replacement (UKR) with total knee replacement (TKR) for simple medial knee OA. Methods: Literature searches of PubMed, Embase, Web of Science, and the Cochrane Library were searched up to 1th April 2020. Only studies comparing UKR with TKR for isolated medial knee OA were included. Data collection and extraction, quality assessment, and data analyses were performed according to the Cochrane standards. Results: A total of 13 articles with 1888 patients were included, among which, 944 and 944 underwent UKR and TKR, respectively. The analyzed postoperative outcomes were mostly within 5 years of follow-up. The meta-analysis showed that UKR improved knee general function (P < 0.00001) and health (P = 0.02), moreover, reduced post-operative pain (P = 0.01) and complications (P < 0.05) more than TKR. There were no significant differences in postoperative revision (P = 0.252), high-activity arthroplasty score (HAAS) (P = 0.307) and Oxford knee score (OKS) (P = 0.15) between the two techniques. Conclusions: The patients of UKR could achieve better clinical results than that of TKR, moreover, there were negligible differences between the two techniques in postoperative revision in the early and mid-term follow-up and surgeons should be aware of the important reasons for revision of UKR. Thus, UKR instead of TKR should be performed in patients with late-stage isolated medial knee OA. [ABSTRACT FROM AUTHOR]

MicroRNAs serve a crucial role in the regulation of malignant biological behavior of Ewing's sarcoma (ES). Abnormal expression of miR-107 has been reported in a cohort of cancers, while its exact function in ES remains unclear. Hence, we explored the expression of miR-107 in ES cells and detected its effects on the malignant phenotype of ES cells. Firstly, we perceived the under-expression of miR-107 in human ES cells contrast with the human mesenchymal stem cells. Over-expression of miR-107 restrained cell proliferation and tube formation, arrested cell cycle progression, and facilitated cell apoptosis in SK-ES-1 and RD-ES cell lines. Furthermore, hypoxia inducible factor-1β (HIF-1β) was assumed as a target gene of miR-107. We confirmed the target role of HIF-1β in ES cells. Finally, restoring the expression of HIF-1β could partly abolish miR-107-mediated tumor suppression in ES cells. In conclusion, our results advised that miR-107 suppressed the malignant biological ability of ES cells through targeting HIF-1β. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) play an important role in the development and progression of endometrial carcinoma (EC). Recently, several studies have shown that microRNA-124 (miR-124) is downregulated in various cancers, which can affect tumor initiation and maintenance. However, the effects of miR-124 on EC are largely unknown. In this study, we identified the under-expression of miR-124 in 35 paired EC tissues and adjacent normal tissues. Further, functional experiments found that ectopic expression of miR-124 markedly suppressed cell proliferation, migration, and invasion of EC cells. It also induced cell apoptosis and G1-phase cell cycle arrest. Moreover, we identified signal transducer and activator of transcription 3 (STAT3) as a direct target of miR-124, and over expression of miR-124 not only induced changes in STAT3 expression but also altered expression of its target genes, cyclin D2 and matrix metalloproteinase 2, in the human endometrial carcinoma cell line HEC-1B. In addition to targeting STAT3 directly, we found that miR-124 suppresses phosphorylation of STAT3 through targeting IL-6R indirectly. Restored STAT3 expression through treatment with IL-6 cytokine partly abolished miR-124-mediated cell cycle arrest and apoptosis induction. These results combined with the tumorigenetic role of STAT3 in HEC-1B cells suggest that the antitumor effects of miR-124 are achieved, at least partly, through down regulation of STAT3 mRNA and its downstream target genes. Therefore, inhibition of constitutively activated STAT3 by ectopic expression of miR-124 in EC may provide a novel therapeutic strategy for the treatment of EC. [ABSTRACT FROM AUTHOR]