Nephroblastoma is the most common renal tumor in children. Abnormal expression of microRNAs (miRs) has been reported to be involved in the progression of various types of cancers. However, the role and underlying mechanism of miR-130b-3p in nephroblastoma remains unknown. Therefore, the present study aimed to explore the role and possible mechanism of miR-130b-3p in nephroblastoma in children. The present study identified that miR-130b-3p was highly expressed in nephroblastoma tissues obtained from children with nephroblastoma. To better understand the functions and the molecular mechanisms of miR-130b-3p in nephroblastoma, TargetScan was used to identify the potential targets of miR-130b-3p. Phosphatase and tensin homolog (PTEN), was identified as a target gene of miR-130b-3p, and it was observed to be downregulated in nephroblastoma. Further analysis indicated that miR-130b-3p inhibitor could significantly reduce cell proliferation, induce apoptosis and suppress the Akt/nuclear factor-κB/survivin signaling pathway in nephroblastoma cells. Notably, all these effects of miR-130b-3p on nephroblastoma cells were reversed by PTEN-small interfering RNA. In summary, the present study suggested that the miR-130b-3p/PTEN axis could serve a critical role in the progression and development of nephroblastoma. It also suggests that miR-130b-3p might be a valuable clinical biomarker and therapeutic target for nephroblastoma in children. Materials and methodsClinical samples. A total of 30 samples of nephroblastoma and normal adjacent tissues were obtained from children with nephroblastoma who had undergone surgery at the
Piperlongumine (PLM) is a natural product from the pods of a plant call Piper longum and was reported to possess antibacterial, antiangiogenic, neuroprotective, anti-inflammatory and anti-tumor activities. However, the role of PLM in inflammatory responses in human Osteoarthritis (OA) chondrocytes has not been yet explored. Thus, in this study, we investigated the anti-inflammatory action of PLM in human OA chondrocytes. Our results demonstrated that PLM treatment effectively reversed IL-1β-inhibited cell viability in a dose-dependent manner. In addition, PLM significantly inhibited the production of NO and PGE2, iNOS and COX-2 expression, as well as suppressed the production of MMP-3 and MMP-13 in IL-1β-stimulated human OA chondrocytes. Furthermore, PLM significantly prevented IL-1β-induced NF-κB activation in human OA chondrocytes. In conclusion, these findings demonstrated that PLM attenuated inflammatory responses in human OA chondrocytes stimulated by IL-1β, possibly through the NF-κB signaling pathway. Thus, PLM may serve as a potential anti-inflammatory agent in the treatment of OA.
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