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1.
Metab Brain Dis ; 39(3): 361-371, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38091240

RESUMO

Circular RNAs (circRNAs) can play essential roles in tumor development, including glioblastoma (GBM). The current study was performed to explore the function and mechanism of circ_0027446 in GBM progression. Circ_0027446, microRNA-346 (miR-346) and Phosphoglycerate kinase 1 (PGK1) levels were detected using reverse transcription-quantitative polymerase chain reaction assay. Cell behaviors were examined using Cell Counting Kit-8 assay, colony formation assay, EdU assay, flow cytometry, and transwell assay. Glycolytic metabolism was analyzed by commercial kits. The protein level was determined via western blot. The target interaction was analyzed by dual-luciferase reporter assay. Circ_0027446 function in vivo was explored by tumor xenograft assay. Circ_0027446 expression was significantly up-regulated in GBM samples and cells. Circ_0027446 down-regulation suppressed proliferation, invasion, glycolytic metabolism and enhanced apoptosis of GBM cells. MiR-346 was a target of circ_0027446, and circ_0027446 promoted GBM progression by sponging miR-346. PGK1 acted as a target gene of miR-346, and circ_0027446 interacted with miR-346 to regulate PGK1 expression. Overexpression of miR-346 inhibited malignant behaviors of GBM cells through down-regulating PGK1. Circ_0027446 contributed to tumor growth in vivo via miR-346/PGK1 axis. The current evidences demonstrated that circ_0027446 facilitated malignant progression of GBM through binding to miR-346 to up-regulate PGK1.


Assuntos
Glioblastoma , MicroRNAs , Humanos , Glioblastoma/genética , Apoptose , Contagem de Células , Regulação para Baixo , MicroRNAs/genética , Proliferação de Células/genética , Linhagem Celular Tumoral , Fosfoglicerato Quinase/genética
2.
Res Vet Sci ; 146: 15-23, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-35298925

RESUMO

The neuropeptide S (NPS) and its receptor (NPSR) represent a signaling system in the brain. Increased levels of NPS and NPSR have been observed in PK15 cells and murine brains in response to pseudorabies virus (PRV) infection, but it remains unclear whether elevated levels of NPS and NPSR are involved in the pathogenic process of PRV infection. In this study, the activities of both NPS and NPSR during PRV pathogenesis were explored in vitro and in vivo by reverse transcription polymerase chain reaction (RT-PCR), PCR, real-time quantitative RT-PCR (qRT-PCR), qPCR, TCID50, and Western blotting methods. NPSR-deficient cells were less susceptible to PRV infection, as evidenced by decreased viral production and PRV-glycoprotein E (gE) expression. In vitro studies showed that exogenous NPS promoted the expression of interleukin 6 (IL-6) mRNA but inhibited interferon ß (IFN-ß) mRNA expression in PK15 cells after PRV infection. In vivo studies showed that NPS-treated mice were highly susceptible to PRV infection, with decreased survival rates and body weights. In addition, NPS-treated mice showed elevated levels of IL-6 mRNA and STAT3 phosphorylation. However, the expression of IFN-ß mRNA was greatly decreased after virus challenge. Contrasting results were obtained from the NPSR-ir-treated groups, which further highlighted the effects of NPS. This study revealed that NPS-treated hosts are more susceptible to PRV infection than controls. Moreover, excessive IL-6/STAT3 and defective IFN-ß responses in NPS-treated mice may contribute to the pathogenesis of PRV.


Assuntos
Herpesvirus Suídeo 1 , Neuropeptídeos , Pseudorraiva , Doenças dos Roedores , Animais , Herpesvirus Suídeo 1/genética , Interleucina-6 , Camundongos , Neuropeptídeos/metabolismo , RNA Mensageiro
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