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Osteoporosis (OP) is a common serious skeletal disorder marked by increased risk of bone fracture due to fragility. OP has been taken to be a disease linked with abnormal calcium metabolism that alone is obviously insufficient to explain the development of OP. Iron overload has been associated with the development of OP and increasing studies have suggested the association. However, direct evidence for this has not been clinically established. To this end, using the Roche biochemical autoanalyzer, we detected the concentration of iron, soluble transferrin receptor 2 (TFR2), and hepcidin, a key peptide regulating iron homeostasis, in the sera from patients with OP. It was shown that the iron and TFR2 concentration was markedly higher than that of healthy control; whereas the concentration of hepcidin was markedly lower than that in control. In addition, to pilot explore the underlying mechanism by which hepcidin was downregulated, we present that hepcidin can directly interact with TFR2 using immunoprecipitation. The present study first established the direct biochemical evidence for the involvement of hepcidin in the pathogenesis of OP, indicating that the upregulation of hepcidin could be used as a novel alternative therapeutic strategy in the management of OP. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether the miR-184 could regulate the proliferation of the tongue squamous cell carcinoma (TSCC) through sex-determining region Y-box 7 (SOX7) gene. miR-184 expression was upregulated in TSCC cell lines and tissues. MTT assay revealed that overexpression of miR-184 significantly promoted the proliferation of the TSCC cells in vitro. SOX7 was the direct target of miR-184 and luciferase reporter assay confirmed that miR-184 downregulated the expression of SOX7. MTT assay verified that knockdown of SOX7 remarkably promoted the proliferation of TSCC cells in vitro. miR-184 promoted the proliferation of TSCC by targeting SOX7. Taken together, our results provided a new potential therapeutic target for TSCC treatment. [ABSTRACT FROM AUTHOR]

Background Gastric cancer (GC) is one of the most common malignant tumor and has high mortality worldwide. microRNAs (miRNAs) play critical roles in carcinogenesis. Previous studied showed that miR-215 was involved in tumorigenesis and progression. This study was designed to clarify the biological function of miR-215 in GC. Methods qRT-PCR was used to detect the miR-215 expression in GC tissues and 6 human GC cell lines (AGS, SGC-7901, NCI-N87, GES-1, MKN-45 and BGC-823) as well. Transwell assay was used to investigate the biological function of miR-215 in GC. Luciferase reporter assay was used to confirm its effect on the regulation of the target gene Retinoblastoma tumor suppressor gene 1 ( RB1 ). Results miR-215 was frequently up-regulated in GC tissues compared to adjacent non-tumor tissues and GC cell lines. miR-215 expression level was correlated with the progression of tumor invasion and tumor-node-metastasis (TNM) stage. Over-expression miR-215 in GC cell lines promoted cell migration and invasion. Besides, miR-215 could down-regulate the expression of RB1 in vitro via directly binding to its 3′-untranslated region (UTR), while the expression of RB1 would suppress the miR-215-indueced GC cell migration and invasion. Conclusions miR-215 promoted cell migration and invasion of gastric cancer by directly targeting RB1 . [ABSTRACT FROM AUTHOR]