RESUMEN
BACKGROUND: Hepatocellular carcinoma (HCC) is a major threat for human health. This work aimed to determine the potential function of circ_0072995 in HCC progression and its molecular mechanism. METHODS: qRT-PCR was conducted to analyze circ_0072995 expression. CCK8 and colony formation assays were utilized to detect cell proliferation. Transwell assay was performed to determine migration and invasion. Interactions among circ_0072995, miR-1253 and EIF4A3 (Eukaryotic Translation Initiation Factor 4A3) were predicted through bioinformatics methods and confirmed via luciferase reporter assay and RNA pulldown assay. RESULTS: circ_0072995 expression was upregulated in HCC tissues. Circ_0072995 high level was associated with poor prognosis. Circ_0072995 knockdown impaired proliferation, migration, invasion and survival. MiR-1253 was sponged by circ_0072995 and targeted EIF4A3 directly. Circ_0072995 inhibited miR-1253 to upregulate EIF4A3 level. CONCLUSION: Circ_0072995 exerted tumorigenic roles to enhance HCC progression through activating EIF4A3 by sponging miR-1253.
RESUMEN
BACKGROUND: Sedum sarmentosum Bunge extract (SSBE) has been used traditionally to treat liver inflammatory diseases in the Asian area. PURPOSE: The aim of this study is to evaluate the anti-inflammatory activity of SSBE on renal injury. METHODS: We investigated whether SSBE has an anti-inflammatory effect by suppressing M1-macrophage polarization in rats with unilateral ureteral obstruction (UUO) and in cultured macrophages. In addition, the effect of SSBE on the activities of interferon regulatory factor-5 (IRF5) and NF-κB p65 were further examined. RESULTS: Oral administration of SSBE (100â¯mg kg-1) markedly inhibited the infiltration of CD68-positive macrophages and reduced tubulointerstitial damage in kidney tissues following injury. In addition, SSBE reduced the expression of proinflammatory cytokine (MIF), chemokine (MCP-1), interleukin (IL-6), IFN-γ, and TNF-α, which are involved in the infiltration and activation of macrophages. Moreover, SSBE treatment also decreased the synthesis and release of MCP-1 and MIF in tubular epithelial cells after injury. Further study revealed that SSBE downregulated the levels of IL-12 and iNOS, indicating a crucial role of SSBE on the inhibition of M1 macrophage polarization in kidney injury. In cultured macrophages, lipopolysaccharide (LPS) induced the polarization of macrophage towards M1 phenotype, but was inhibited by SSBE treatment. Notably, SSBE reduced the activities of interferon regulatory factor 5 (IRF5) and NF-κB p65 in injured kidneys and in LPS-treated macrophages, which was independent of TLR4/MyD88. As a result, SSBE reduced the expression of HIF-1α and the induction of GLUT1, and thereby inhibited anaerobic glycolysis in macrophages. CONCLUSION: SSBE exerts a marked anti-inflammatory effect and alleviates kidney injury, at least in part, by suppressing M1-macrophage polarization.