&lt;p&gt;Long noncoding RNA ZEB2-AS1 facilitates laryngeal squamous cell carcinoma progression by miR-6840-3p/PLXNB1 axis&lt;/p&gt;

et al. 2021

Front. Mol. Biosci.

BackgroundHepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is a life-threatening disease with a high mortality rate; the systemic inflammatory response plays a vital role in disease progression. We aimed to determine if a miRNA–mRNA co-regulatory network exists in the peripheral blood mononuclear cells (PBMCs) of HBV-ACLF patients, which might be important for prognosis.MethodsIn patients with HBV-ACLF meeting COSSH-ACLF criteria, age, liver cirrhosis and INR were independent risk factors for 28-day and 90-day poor prognosis. COSSH-ACLFs was a superior prognostic model. mir-6840-3p-JADE2 may promote the progression of ACLF and lead to poor prognosis. Meanwhile, mir-6840-3p and mir-6861-3p can be used as markers of short-term poor prognosis. Finally, ALSS treatment is not only the blood material exchange of patients, but also changes part of the immune state of patients. Among them, cytokine cytokine receptor interaction may play an important role in determining the therapeutic effect.MethodsTranscriptome-wide microRNA (miRNA) and mRNA microarrays were used to define the miRNA and mRNA expression profiles of the PBMCs of HBV-ACLF patients in a discovery cohort. The targets of the miRNAs were predicted. We built a miRNA-mRNA regulatory network through bioinformatics analysis, and used quantitative real-time polymerase chain reaction (qRT-PCR) to assess the importance of candidate miRNAs and mRNAs. We also assessed the direct and transcriptional regulatory effects of miRNAs on target mRNAs using a dual-luciferase reporter assay.ResultsThe miRNA/mRNA PBMC expression profiles of the discovery cohort, of whom eight survived and eight died, revealed a prognostic interactive network involving 38 miRNAs and 313 mRNAs; this was constructed by identifying the target genes of the miRNAs. We validated the expression data in another cohort, of whom 43 survived and 35 died; miR-6840-3p, miR-6861-3p, JADE2, and NR3C2 were of particular interest. The levels of miR-6840-3p and miR-6861-3p were significantly increased in the PBMCs of the patients who died, and thus predicted prognosis (areas under the curve values = 0.665 and 0.700, respectively). The dual-luciferase reporter assay indicated that miR-6840-3p directly targeted JADE2.ConclusionWe identified a prognostic miRNA-mRNA co-regulatory network in the PBMCs of HBV-ACLF patients. miR-6840-3p-JADE2 is a potential miRNA–mRNA pair contributing to a poor prognosis.

Section: Discussionmentioning

confidence: 99%

Identification of a Potential miRNA–mRNA Regulatory Network Associated With the Prognosis of HBV-ACLF

Xie

et al. 2021

Front. Mol. Biosci.

“…PLXNB1 is a member of plexins which bind to ligands called semaphorins. 35 Depletion of PLXNB1 represses lipopolysaccharide-triggered chondrocyte injury, thereby attenuating OA pathogenesis. 36 A previous report also showed low PLXNB1 expression in the trabecular bones of OA patients.…”

Section: Discussionmentioning

confidence: 99%

MiR-362-5p inhibits cartilage repair in osteoarthritis via targeting plexin B1

J Orthop Surg (Hong Kong)

et al. 2022

Background and objectives Chondrogenesis of bone marrow mesenchymal stem cells (BMSCs) exerts great function during the pathogenesis of osteoarthritis (OA). Studies have reported the association of plexin B1 (PLXNB1) with OA pathogenesis. In this study, the upstream mechanism and function of PLXNB1 in this disease were explored. Methods Flow cytometry was applied to test BMSC characterization. Chondrogenic differentiation of BMSCs was evaluated by Alcian blue staining. The expression of PLXNB1, miR-362-5p, miR-501-5p, miR-1827, miR-500-5p was measured using RT-qPCR analysis. The protein levels of PLXNB1, Aggrecan, and Silent information regulator factor 2-related enzyme 1 (SIRT1) were determined by western blotting. Binding relationship between miR-362-5p and PLXNB1 was confirmed using bioinformatics analysis and luciferase reporter assay. The in vivo model of OA was established in Sprague-Dawley rats which received medial meniscus instability surgery. For histopathological examination, cartilage tissues in the knee joint of rats were stained with hematoxylin and eosin. Micro-CT analysis was employed to observe the changes of morphometric indices including average trabecular separation, average trabecular thickness, and bone volume fraction. Results BMSCs were identified to possess the characteristics of mesenchymal stem cells. PLXNB1 was observed to be highly expressed during chondrogenic differentiation of BMSCs and PLXNB1 overexpression promoted BMSC chondrogenic differentiation. Mechanically, PLXNB1 was targeted by miR-362-5p. In rescue assays, miR-362-5p reversed the effects of PLXNB1 on chondrogenic differentiation of BMSCs. In the in vivo experiments, upregulated PLXNB1 expression alleviated joint injury of OA rats. Additionally, overexpressed miR-362-5p and downregulated PLXNB1 expression levels were detected in OA rats. Conclusion MiR-362-5p promotes OA progression by suppressing PLXNB1.

“…Growing researches have demonstrated that LINC01638 interacts with miRNA to regulate tumorigenesis [ 6 , 16 ]. For instance, lncRNA ZEB2-AS1 sponges miR-6840-4p to facilitate LSCC progression [ 20 ]. LncRNA NEAT1 enhances LSCC development by targeting miR-107/CDK6 axis [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC01638 contributes to laryngeal squamous cell cancer progression by modulating miR-523-5p/BATF3 axis

Zhao

Wang

et al. 2021

Aging

Long noncoding RNA (lncRNA) plays a critical role in tumorigenesis. How lncRNA regulates laryngeal squamous cell carcinoma (LSCC) progression remains poorly understood. In the present study, we found that LINC01638 was highly expressed in LSCC tissues. And LINC01638 expression was positively correlated with clinical stage and lymph node metastasis. Patients with LINC01638 high expression displayed a low survival rate. Results from CCK8, colony formation, and transwell assays showed that LINC01638 knockdown suppressed the proliferation, migration and invasion of LSCC cells in vitro . Animal experiments indicated that LINC01638 silencing attenuated tumor growth in vivo . In terms of mechanism, LINC01638 was found to sponge miR-523-5p and promote BATF3 expression. In summary, our results demonstrated that LINC01638/miR-523-5p/BATF3 axis plays a crucial function in initiating LSCC development and may be a potential target for tumor therapy.