PSMB8 regulates glioma cell migration, proliferation, and apoptosis through modulating ERK1/2 and PI3K/AKT signaling pathways

Yang, Bo; Song, Jingwei; Sun, Hongmei; Xing, Jing; Yang, Zhihui; Wei, Changyong; Xu, Tianhua; Yu, Zhiyang; Zhang, Yenan; Wang, Ying-fan; Chang, Hao; Xu, Zhipeng; Hou, Min; Ji, Minjun; Zhang, Yansong

doi:10.1016/j.biopha.2018.01.170

Cited by 49 publications

(52 citation statements)

References 21 publications

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“…Overexpression of miR‐451 suppresses PSMB8, NOS2, VEGF, MMP‐2, and MMP‐9, which may suppress the growth and migration of the lung cancer cell line A549 18 . In addition, PSMB8 reduces migration, proliferation, and apoptosis through the ERK1/2 and PI3K/AKT signaling pathways in U87MG cells 11 . In our previous study, knockdown of PSMB4 expression reduced the levels of integrin β1, β3, p‐FAK, MMP2, and MMP9 in LN229 cells.…”

Section: Discussionmentioning

confidence: 99%

“…PSMB8 overexpression correlates with gastric cancer progression, especially aspects related to the depth of tumor invasion and lymph node metastasis 10 . In glioblastoma, PSMB8 inhibition induces apoptosis and blocks migration and invasion via PI3K/AKT regulation 11 . However, whether PSMB8 regulates angiogenesis and the underlying mechanisms in GBM remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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PSMB8 inhibition decreases tumor angiogenesis in glioblastoma through vascular endothelial growth factor A reduction

et al. 2020

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Glioblastoma, also known as glioblastoma multiforme (GBM), is a fast‐growing tumor and the most aggressive brain malignancy. Proteasome subunit beta type‐8 (PSMB8) is one of the 17 essential subunits for the complete assembly of the 20S proteasome complex. The aim of the present study was to evaluate the role of PSMB8 expression in GBM progression and angiogenesis. PSMB8 expression in glioblastoma LN229 and U87MG was knocked down by siRNA or inducible shRNA both in vitro and in vivo. After PSMB8 reduction, cell survival, migration, invasion, angiogenesis, and the related signaling cascades were evaluated. An orthotopic mouse tumor model was also provided to examine the angiogenesis within tumors. A GEO profile analysis indicated that high expression of PSMB8 mRNA in GBM patients was correlated with a low survival rate. In immunohistochemistry analysis, PSMB8 expression was higher in high‐grade than in low‐grade brain tumors. The proliferation, migration, and angiogenesis of human GBM cells were decreased by PSMB8 knockdown in vitro. Furthermore, phosphorylated focal adhesion kinase (p‐FAK), p‐paxillin, MMP2, MMP9, and cathepsin B were significantly reduced in LN229 cells. Integrin β1 and β3 were reduced in HUVEC after incubation with LN229‐conditioned medium. In an orthotopic mouse tumor model, inducible knockdown of PSMB8 reduced the expression of vascular endothelial growth factor (VEGF), VEGF receptor, and CD31 as well as the progression of human glioblastoma. In this article, we demonstrated the role of PSMB8 in glioblastoma progression, especially neovascularization in vitro and in vivo. These results may provide a target for the anti–angiogenic effect of PSMB8 in glioblastoma therapy in the future.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

PSMB8 inhibition decreases tumor angiogenesis in glioblastoma through vascular endothelial growth factor A reduction

et al. 2020

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“…Yun et al showed that the downregulation of CAPG significantly inhibited GBM cell proliferation by blocking the cell cycle in G1/S transition [ 37 ]. PSMB8, a protein contributes to the complete assembly of 20S proteasome complex, regulates glioma cell migration, proliferation, and apoptosis [ 38 ]. Previous study shows that autoinflammatory disorder caused by PSMB8 mutation leads to the proteasome assembly defection [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA

Yang

Wang

Wei

et al. 2018

BioMed Research International

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To reveal the potential molecular mechanism of glioblastoma multiforme (GBM) and provide the candidate biomarkers for GBM gene therapy. Microarray dataset GSE50161 was obtained from GEO database. The differentially expressed genes (DEGs) were identified between GBM samples and control samples, followed by the module partition analysis based on WGCNA. Then, the pathway and functional enrichment analyses of DEGs were performed. The hub genes were further investigated, followed by the survival analysis and data validation. A total of 1913 DEGs were investigated between two groups, followed by analysis of 5 modules using WGCNA. These DEGs were mainly enriched in functions like inflammatory response. The hub genes including upregulated N-Myc and STAT Interactor (NMI), Capping Actin Protein-Gelsolin Like (CAPG), and Proteasome Subunit Beta 8 (PSMB8) were revealed as potential liquid biopsy molecules for GBM diagnose. Moreover, Nucleolar and Spindle Associated Protein 1 (NUSAP1) and G Protein-Coupled Receptor 65 (GPR65) were outstanding genes in survival analysis. Our results suggested that CPNE6, HAPLN2, CMTM3, NMI, CAPG, and PSMB8 might be used as potential molecules for liquid biopsy of GBM. NUSAP1 and GPR65 might be novel prognostic targets for GBM gene therapy. Furthermore, the upregulated NMI might play an important role in GBM progression via inflammatory response.

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“…Many studies have shown that proteasome subunit beta type 8 gene (PSMB8) participates in the PI3K-Akt signalling pathway, and is involved in various diseases such as glioma, LAML, DKD, etc. [28][29] .…”

Section: Discussionmentioning

confidence: 99%

Potential Biomarkers of Diabetic Kidney Disease Based on Weighted Gene Co-expression Network Analysis

Chen¹,

Xiao²,

Shi³

et al. 2020

Preprint

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Background: Diabetic kidney disease (DKD) is one of the serious complications of diabetes. However, there is no unified and clear understanding of the pathogenesis of DKD at present. The evidence suggests that genetic predispositions play a significant role in an individual’s susceptibility to DKD. WGCNA analysis may provide a new way to search for genes closely related to DKD. Methods: In this study we analysed key genes and pathways involved in DKD from RNA-seq count results using 23 peripheral blood samples from patients with DKD. Weighted gene co-expression network analysis (WGCNA) was performed with the WGCNA package.Results: We found turquoise and purple module were characterized as having the highest correlation with large proteinuria stage in DKD. Furthermore, the key genes, including DCN, F2R, LTBP2, B2M, PSMB8, and NLRC5, were evaluated through a protein-protein interaction (PPI) network combined with a co-expression network, which were expected to be potential diagnostic and therapeutic targets of DKD. Conclusions: These signalling pathways and hub genes will provide effective targets and ideas for further study of the pathogenesis of DKD and are expected to have roles in the prevention of, early screening for, and the treatment of DKD.

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PSMB8 regulates glioma cell migration, proliferation, and apoptosis through modulating ERK1/2 and PI3K/AKT signaling pathways

Cited by 49 publications

References 21 publications

PSMB8 inhibition decreases tumor angiogenesis in glioblastoma through vascular endothelial growth factor A reduction

PSMB8 inhibition decreases tumor angiogenesis in glioblastoma through vascular endothelial growth factor A reduction

Candidate Biomarkers and Molecular Mechanism Investigation for Glioblastoma Multiforme Utilizing WGCNA

Potential Biomarkers of Diabetic Kidney Disease Based on Weighted Gene Co-expression Network Analysis

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