Quercetin can suppress osteosarcoma cell growth and metastasis. However, other effects of quercetin on osteosarcoma remain largely unknown. This research aims to evaluate the effects of quercetin in combination with cisplatin as treatment for osteosarcoma and investigate its regulatory mechanism. Cell viability and apoptosis in 143B cell line were determined after treatment with quercetin and/or cisplatin. RT-PCR and Western blot analysis were performed to determine the RNA or protein expression levels. Moreover, transwell assay was used to evaluate metastasis. Furthermore, rescue experiments were performed to investigate the potential regulatory mechanism of the treatment. Results showed that quercetin with concentration that was equal to or greater than 10 μM inhibited 143B proliferation, while 5 μM quercetin enhanced the cisplatin sensitivity of 143B cells. Expression of miR-217 was upregulated after quercetin and/or cisplatin treatment, while its target KRAS was downregulated both at mRNA and protein levels. MiR-217 knockdown led to the loss of enhanced cisplatin sensitivity while miR-217 overexpression showed the opposite effects, indicating that quercetin regulated cisplatin sensitivity by modulating the miR-217-KRAS axis. In conclusion, 5 μM quercetin enhanced the cisplatin sensitivity by modulating the miR-217-KRAS axis. This finding suggests that quercetin may be administered with cisplatin to improve the treatment for osteosarcoma.

This is an Open Access article distributed under the terms of the Creative Commons Attribution NonCommercial License (http://creativecommons.org/ licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.Purpose: This study is intended to investigate the effects of plants or plant-derived antioxidants on prevention of osteoporosis through the maintenance of reactive oxygen species (ROS) at a favorable level. Materials and Methods: In this study, a novel antioxidant, namely 3,4,5-Trihydroxy-N-[4-(5-hydroxy-6-methoxy-pyrimidin-4-ylsulfamoyl)-phenyl]-benzamide (ZXHA-TC) was synthesized from gallic acid and sulfadimoxine. Its effect on osteoblast metabolism was investigated via the detection of cell proliferation, cell viability, production of ROS, and expression of osteogenic-specific genes including runt-related transcription factor 2 (RUNX2), bone sialoprotein (BSP), osteocalcin (OCN), alpha-1 type I collagen (COL1A1), and osteogenic-related proteins after treatment for 2, 4, and 6 days respectively. Results:The results showed that ZXHA-TC has a stimulating effect on the proliferation and osteogenic differentiation of primary osteoblasts by promoting cell proliferation, cell viability, and the expression of genes BSP and OCN. Productions of bone matrix and mineralization were also increased by ZXHA-TC treatment as a result of up-regulation of COL1A1 and alkaline phosphatase (ALP) at the early stage and down-regulation of both genes subsequently. A range of 6.25×10 -3 μg/mL to 6.25×10 -1 μg/mL is the recommended dose for ZXHA-TC, within which 6.25×10 -2 μg/mL showed the best performance. Conclusion: This study may hold promise for the development of a novel agent for the treatment of osteoporosis.

Mitochondrial ribosomal protein S23 (MRPS23), encoded by a nuclear gene, is a participant in the translation of mitochondrial proteins. Recently, MRPS23 has been reported to be overexpressed in many types of cancers and have a close association with cancer progression. However, the specific roles of MRPS23 in osteosarcoma (OS) remain unknown. In this study, we investigated the expression pattern and biological functions of MRPS23 in OS cells. Our results demonstrated that MRPS23 was up-regulated in OS tissues and cell lines. Down-regulation of MRPS23 significantly inhibited OS cell proliferation and invasion induced by lipopolysaccharide (LPS) in vitro. Furthermore, the in vivo experiments showed that MRPS23 down-regulation markedly suppressed OS cell growth and metastasis induced by LPS. Mechanistically, down-regulation of MRPS23 inhibited the activity of NF-kB signaling pathway in OS cells. In conclusion, these findings indicated that MRPS23 may be a potential therapeutic target for OS treatment. Results Expression of MRPS23 is elevated in OS tissues and cell linesThe expression of MRPS23 in OS tissues was examined by immunohistochemistry, RT-PCR and western blot analysis. The

Retraction of ‘Down-regulation of MRPS23 inhibits LPS-induced proliferation and invasion via regulation of the NF-κB signaling pathway in osteosarcoma cells’ by Ai-Guo Liu et al., RSC Adv., 2019, 9, 10561–10568, https://doi.org/10.1039/C8RA08973F.