BackgroundMounting evidence has revealed that abnormal expression of circular RNAs play pivotal roles in many human diseases including preeclampsia (PE). While human sapiens circular RNA 0007121 (hsa_circ_0007121) has been verified to be downregulated in human placental tissues, the underlying mechanisms were still unclear. This research aims to investigate the effect and underlying mechanisms of hsa_circ_0007121 in preeclampsia.MethodsThe expression of hsa_circ_0007121, microRNA (miR)-182-5p, and placental growth factor (PGF) was assessed by quantitative reverse transcription polymerase chain reaction in PE placentas relative to the expression in normal pregnancy placentas. After transfection, cell counting kit-8 assay was employed to detect cell proliferation. Cell migration and invasion were tested by the transwell assay. The relative level of epithelial–mesenchymal transition (EMT)-related proteins in HTR-8/SVneo cells and PGF in placentas samples were measured by western blot. The relationship between miR-182-5p and hsa_circ_0007121 or PGF was predicated by circular RNA interactome or ENCORI and verified by dual-luciferase reporter assay and RNA immunoprecipitation assay.ResultsThe levels of hsa_circ_0007121 and PGF were significantly declined in PE placental tissues and HTR-8/SVneo cells, whereas miR-182-5p had an opposite result. Downregulation of hsa_circ_0007121 obviously inhibited HTR-8/SVneo cell proliferation, migration, invasion, and EMT, while upregulation of hsa_circ_0007121 promoted this process. Besides, miR-182-5p was a target gene of hsa_circ_0007121 and could target PGF. Further analysis indicated that hsa_circ_0007121 regulated the proliferation, migration, invasion, and EMT of HTR-8/SVneo cells via altering PGF expression by interacting with miR-182-5p.ConclusionHsa_circ_0007121 mediated the progression of PE via miR-182-5p/PGF axis.

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In this study, the function of long non-coding RNA SOX21 antisense RNA 1 (SOX21-AS1) in the progress of glioma was explored. RNA and protein levels were measured via quantitative reverse transcription-PCR (qRT-PCR) and western blot analysis. In addition, we examined cell proliferation, apoptosis, migration and invasion. The interaction between SOX21-AS1 (PAK7) and miR-144-3p was determined via RNA immunoprecipitation (RIP) assay and Luciferase reporter assay. SOX21-AS1 was upregulated in glioma tissues and cells. SOX21-AS1 knockdown was carried out in glioma cells (U251 and U87 cells). Moreover, in vitro, SOX21-AS1 knockdown repressed proliferation, migration, invasion and enhanced apoptosis in glioma cells. In vivo, SOX21-AS1 knockdown suppressed tumor growth in mice. In addition, SOX21-AS1 could sponge miR-144-3p, which was determined to bind to PAK7. miR-144-3p knockdown promoted proliferation, migration, invasion and inhibited cell apoptosis. Importantly, the effects of SOX21-AS1 knockdown-induced proliferation, migration, invasion, and apoptosis were alleviated in glioma cells co-transfected with SOX21-AS1 and miR-144-3p knockdown. Furthermore, miR-144-3p knockdown also attenuated Wnt/β-catenin pathway-associated protein levels induced by SOX21-AS1 knockdown. These results indicated that SOX21-AS1/miR-144-3p/PAK7 axis played an oncogenic role in glioma cells by regulating Wnt/β-catenin pathway, which suggests a rational therapeutic strategy for glioma.

<b><i>Background:</i></b> Asperulosidic acid (ASP) is a bioactive iridoid exerting broad pharmacological and medicinal properties. However, it is still unknown if ASP has therapeutical effects on gestational diabetes mellitus (GDM). This study aims to evaluate the effects of ASP on GDM as well as its underlying mechanism. <b><i>Methods:</i></b> A mouse model of GDM was established and orally administrated ASP (10, 20, and 40 mg/kg) on gestation day (GD) 0. The mice were sacrificed on GD 18. <b><i>Results:</i></b> Blood glucose and serum insulin were then determined. The inflammatory cytokines including IL-6 and TNF-α and oxidative stress biomarkers including MDA, SOD, GSH, and GPx were determined by using specific ELISAs. In addition, the expressions of NF-κB and MAPK signaling pathway-related proteins were determined by using Western blotting. Treatment with ASP decreased blood glucose in the mouse model of GDM. Besides, ASP also increased serum insulin and attenuated β-cell function. Treatment with ASP suppressed IL-6 and TNF-α and regulated oxidative stress-related biomarkers. Western blotting analysis showed that treatment with ASP suppressed phosphorylation of NF-κB p65, ERK1/2, and p38 in placental tissues. <b><i>Conclusion:</i></b> ASP alleviates placental oxidative stress and inflammatory responses in GDM by the inhibition of the NF-κB and MAPK signaling pathways.