The role of cullin proteins in gastric cancer

Chen, Peng; Yao, Guo‐Dong

doi:10.1007/s13277-015-4154-z

Cited by 16 publications

(8 citation statements)

References 108 publications

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“…High antigen KI-67 and CUL5 expression levels in tissues are associated with cancers [44,[52][53][54][55][56]. We observed increased serum concentrations of these proteins in patients with CKD in this study.…”

Section: Discussionsupporting

confidence: 60%

Proteomic Analysis of Human Serum from Patients with Chronic Kidney Disease

et al. 2020

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Chronic kidney disease (CKD) is an important public health problem in the world. The aim of our research was to identify novel potential serum biomarkers of renal injury. ELISA assay showed that cytokines and chemokines IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12 (p70), IL-13, IL-15, IL-17, Eotaxin, FGFb, G-CSF, GM-CSF, IP-10, MCP-1, MIP-1α, MIP-1β, PDGF-1bb, RANTES, TNF-α and VEGF were significantly higher (R > 0.6, p value < 0.05) in the serum of patients with CKD compared to healthy subjects, and they were positively correlated with well-established markers (urea and creatinine). The multiple reaction monitoring (MRM) quantification method revealed that levels of HSP90B2, AAT, IGSF22, CUL5, PKCE, APOA4, APOE, APOA1, CCDC171, CCDC43, VIL1, Antigen KI-67, NKRF, APPBP2, CAPRI and most complement system proteins were increased in serum of CKD patients compared to the healthy group. Among complement system proteins, the C8G subunit was significantly decreased three-fold in patients with CKD. However, only AAT and HSP90B2 were positively correlated with well-established markers and, therefore, could be proposed as potential biomarkers for CKD.

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Section: Discussionsupporting

confidence: 60%

Proteomic Analysis of Human Serum from Patients with Chronic Kidney Disease

et al. 2020

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“…Moreover, CUL7 overexpression promoted proliferation in glioma cells in our study. Although many previous studies have reported that CUL7 promoted tumorigenesis by suppressing P53 [10,40,41], CUL7 also promoted the proliferation of U251, a glioma cell line with mutated p53 [42], in our study; this indicates that CUL7 could have other independent pathways to promote the development of glioma. In this way, to attain the potential molecular mechanisms by which CUL7 promotes glioma development, we detected the expression changes of some key mediators of cell proliferation and apoptosis, including p21, p27, cyclin D1, CDK4, cyclin E1 and CDK2.…”

Section: Discussioncontrasting

confidence: 79%

Cullin-7 (CUL7) is overexpressed in glioma cells and promotes tumorigenesis via NF-κB activation

Zhang

Qian

et al. 2020

J Exp Clin Cancer Res

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Background: Cullin-7 (CUL7) is a member of the DOC domain-containing cullin family and is involved in the regulation of cell transformation. However, the clinical significance, potential mechanism and upstream regulators of CUL7 in malignant gliomas remain to be determined. Methods:Expression level data and clinical information were obtained via the Cancer Genome Atlas (TCGA) database, the Chinese Glioma Genome Atlas (CGGA) database, immunohistochemistry (IHC) and western blot analysis. Gene set enrichment analysis (GSEA) was used to explore the potential molecular mechanisms of CUL7. RNA silencing was performed using siRNA or lentiviral constructs in U87MG and U251 glioma cell lines and GSC267 glioma stem cells. CUL7 overexpression was performed using the GV141-CUL7 plasmid construct. In addition, overexpression of miR-3940-5p was performed and validated by quantitative real-time PCR (qRT-PCR). Cells were characterized in vitro or in vivo to evaluate their molecular status, cell proliferation, invasion, and migration by Cell Counting Kit (CCK)-8, EdU, flow cytometry, colony formation, Transwell and 3D tumour spheroid invasion assays. Coimmunoprecipitation (co-IP) and western blotting were performed to test the mechanisms of activation of the NF-κB signalling pathway.Results: High CUL7 expression was associated with a high tumour grade, a mesenchymal molecular glioma subtype and a poor prognosis in patients. Gene silencing of CUL7 in U87MG and U251 cells significantly inhibited tumour growth, invasion and migration in vitro and in vivo. Western blot analysis revealed that cyclin-dependent kinase inhibitors and epithelial-mesenchymal transition (EMT) molecular markers changed under CUL7 silencing conditions. In contrast, CUL7 overexpression promoted tumour growth, invasion and migration. Gene set enrichment analysis (GSEA) and western blot analysis revealed that CUL7 was positively associated with the NF-κB pathway. Moreover, with coimmunoprecipitation assays, we discovered that CUL7 physically associated with MST1, which further led to ubiquitin-mediated MST1 protein degradation, which promoted activation of the NF-κB signalling pathway. Finally, CUL7 was found to be downregulated by miR-3940-5p, which suppressed the development of gliomas.(Continued on next page)

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“…Cul2 has been predicted to be a tumor suppressor protein because of its association with the von Hippel-Lindau gene and ubiquitinated HIFa degradation (18,19). However, it has also been reported that Cul2 is required for normal vasculogenesis and involved in cell-cycle regulation (20) and that it promotes gastric cancer progression (35,36). In our study, we analyzed 75 HCC tissues, and the results showed that the Cul2 expression level was not significantly correlated with HCC metastasis.…”

Section: Discussionmentioning

confidence: 71%

Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma

et al. 2018

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Twist is a critical epithelial-mesenchymal transition (EMT)-inducing transcription factor that increases expression of vimentin. How Twist1 regulates this expression remains unclear. Here, we report that Twist1 regulates Cullin2 (Cul2) circular RNA to increase expression of vimentin in EMT. Twist1 bound the Cul2 promoter to activate its transcription and to selectively promote expression of Cul2 circular RNA (circ-10720), but not mRNA. circ-10720 positively correlated with Twist1, tumor malignance, and poor prognosis in hepatocellular carcinoma (HCC). Twist1 promoted vimentin expression by increasing levels of circ-10720, which can absorb miRNAs that target vimentin. circ-10720 knockdown counteracted the tumor-promoting activity of Twist1 and in patient-derived xenograft and diethylnitrosamine-induced TetOn-Twist1 transgenic mouse HCC models. These data unveil a mechanism by which Twist1 regulates vimentin during EMT. They also provide potential therapeutic targets for HCC treatment and provide new insight for circular RNA (circRNA)-based diagnostic and therapeutic strategies. A circRNA-based mechanism drives Twist1-mediated regulation of vimentin during EMT and provides potential therapeutic targets for treatment of HCC. http://cancerres.aacrjournals.org/content/canres/78/15/4150/F1.large.jpg .

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The role of cullin proteins in gastric cancer

Cited by 16 publications

References 108 publications

Proteomic Analysis of Human Serum from Patients with Chronic Kidney Disease

Proteomic Analysis of Human Serum from Patients with Chronic Kidney Disease

Cullin-7 (CUL7) is overexpressed in glioma cells and promotes tumorigenesis via NF-κB activation

Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma

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