Luteolin (3,4,5,7-tetrahydroxyflavone) is a natural flavonoid that has been found to exhibit anticancer properties in certain types of cancers. In the present study, the role of luteolin and its underlying mechanisms were explored in colorectal cancer (CRC) cells. First, the effects of luteolin on CRC cells proliferation, migration and invasion were examined by CCK-8, wound healing and Transwell assays, respectively. It was demonstrated that luteolin had no effects on CRC cells proliferation while inhibited cells migration and invasion both in vitro and in vivo . Then, expression of pleiotrophin (PTN) and miR-384 was detected in cells and CRC tissues by qPCR. Luteolin was found to upregulate miR-384 and downregulate PTN expressions both in CRC cells and tissues. miR-384 inhibition and PTN overexpression partially reversed the inhibition of HT-29 cells migration and invasion induced by luteolin. Target analysis revealed that miR-384 directly regulates PTN expression. The correlation analysis between PTN expression and clinical characteristics revealed that PTN expression was positively related to cancer progression. The present study demonstrated that luteolin exerts anticancer effects against CRC cells by modulating PTN via miR-384 expression suggested that PTN may serve as a promising candidate for therapeutic applications in CRC treatment.
Hyperlipidemia is associated with metastasis in patients with gastric cancer (GC). 25-Hydroxycholesterol (25-HC) is a type of oxysterol which is synthesized from cholesterol and is involved in a number of processes, including inflammation, immune responses and cancer development. However, the role of 25-HC in gastric cancer remains unknown. In the present study, we demonstrated that 25-HC had no effects on GC cell proliferation and apoptosis, whereas it decreased the sensitivity of GC cells to 5-fluorouracil (5-FU), as demonstrated by the increased cell proliferation and the decreased cell apoptosis. On the other hand, exposure to 2.5-10 µM of 25-HC significantly promoted GC invasion, both in vitro (using AGS and MGC-803 GC cell lines) and in vivo (in an animal model), accompanied by the upregulation of the expression levels of matrix metalloproteinases (MMPs). Further investigations revealed that the promotion of GC invasion was, at least in part due to the activation of Toll-like receptor 2 (TLR2)/nuclear factor (NF)-κB signaling. Our results demonstrated that 25-HC promoted GC cells invasion by upregulating TLR2/NF-κB-mediated MMP expression. Thus, on the whole, the findings of this study suggest a novel mechanism of hyperlipidemia-induced GC progression.
Background: 18β-glycyrrhetinic acid (18β-GA) is reported to possess various pharmacological properties of which anti-inflammatory activities has been widely explored. However, the role of 18β-GA in Staphylococcus aureus (SA) infection has not been investigated. The aim of the present study was to explore the effects of 18β-GA on the SA infection especially the SA-induced Acute lung injury (ALI) and its related mechanisms. Material and methods: We infected the mice or cells with SA and then detected the survival rates of mice, bacterial burden and production of proinflammatory cytokines both in vitro and in vivo. We then detected the High-mobility group box 1 (HMGB1) expression by RT-qPCR and Western blotting. The effects on NF-κB activation was also determined by Western blotting and luciferase assay. Results: 18β-GA could significantly improve the survival rate of SA-infected mice, reduce bacterial burden, suppress infiltration of inflammatory cells and reduce secretion of IL-1β, IL-6 and TNF-α both in lung tissues and cells. 18β-GA treatment decreased high-mobility group box 1 (HMGB1) expression induced by SA infection and neutralizing of HMGB1 could improve the survival rate of mice induced by SA, implying that 18β-GA protected SA infection through down-regulating HMGB1 expression. Finally, we demonstrated that 18β-GA inhibited the NF-κB activation. Conclusion: Taken together, our preliminary study suggested that 18β-GA provided protective effects against SA infection via its antiinflammatory properties possibly through down-regulating the HMGB1/NF-κB activation.
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