The involvement of nuclear factor-κappaB in the nuclear targeting and cyclin E1 upregulating activities of hepatoma upregulated protein

Chen, Jo Mei Maureen; Chiu, Shao‐Chih; Wei, Tong; Lin, Shing-Jong; Chong, Cheong Meng; Wu, Chi Chen; Huang, Jiao Ying; Yang, Shu; Ku, Chia Feng; Hsia, Jiun-Yi; Yu, Chang Tze Ricky

doi:10.1016/j.cellsig.2014.09.020

Cited by 13 publications

(20 citation statements)

References 48 publications

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“…Collectively, our clinical data and in vitro studies suggested that HURP may promote carcinogenesis in multiple ways. These findings corroborated the initial conclusions of Chen et al ( 14 ). The authors found that HURP was phosphorylated by AURKA and shuttled from the cytoplasm to the nucleus and engaged in the regulation of cyclin E1 expression by combining with NFκB.…”

Section: Discussionsupporting

confidence: 92%

“…Yu et al ( 6 ) found that HURP could shuttle from the cytoplasm to the nucleus to avoid degradation. Chen et al ( 14 ) further confirmed that HURP enters into the nucleus through the nuclear localization signal and is engaged in the regulation of cyclin E1 expression as a co-transcription factor. From the above findings, HURP was confirmed as a putative oncoprotein that promotes carcinogenesis through various molecular mechanisms.…”

Section: Introductionmentioning

confidence: 92%

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Prognostic and predictive value of HURP in non‑small cell lung cancer

et al. 2018

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Previous studies have revealed that HURP (also known as DLGAP5 or KIAA0008) is overexpressed in many types of human cancers, such as hepatocellular carcinoma, squamous cell bladder cancer, and transitional cell carcinoma, indicating that HURP is a putative oncoprotein that promotes carcinogenesis through various molecular mechanisms. However, the role of HURP in the pathogenesis of non-small cell lung cancer (NSCLC) has not been reported. In the present study, we investigated the prognostic value of HURP among NSCLC patients through the GEO database. The online tool of KM-plotter was used to identify the correlation of HURP expression and the survival of NSCLC patients. We found the HURP expression at the mRNA level was correlated with the clinicopathologic characteristics and prognosis of NSCLC patients. HURP was highly expressed in aggressive NSCLC cells, and its higher expression was associated with shorter survival. Further cytological experiments revealed that the silencing of HURP caused cell cycle arrest and inhibited the proliferation of NSCLC cells. Transwell assay showed that HURP shRNA inhibited cell migration and invasion in vitro. The bioinformatic analysis suggests that HURP promotes carcinogenesis in multiple manners. Taken together, we revealed the prognostic value of HURP in NSCLC patients and HURP may be a potential therapeutic target for NSCLC.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 92%

Prognostic and predictive value of HURP in non‑small cell lung cancer

et al. 2018

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“…Inhibition of PDE4 elevates intracellular cAMP levels, which inhibit the activity of promoters such as NF-κB and down-regulation of the inflammatory responses by reducing the expression of TNF-α and other pro-inflammatory cytokines, while increasing anti-inflammatory cytokines such as IL-10 [ 91 ]. Interestingly, PDE4 inhibition is used as therapeutics for the treatment of inflammatory diseases in numerous studies [ 92 , 93 ]…”

Section: Discussionmentioning

confidence: 99%

Integration of machine learning and meta-analysis identifies the transcriptomic bio-signature of mastitis disease in cattle

et al. 2018

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Gram-negative bacteria such as Escherichia coli (E. coli) are assumed to be among the main agents that cause severe mastitis disease with clinical signs in dairy cattle. Rapid detection of this disease is so important in order to prevent transmission to other cows and helps to reduce inappropriate use of antibiotics. With the rapid progress in high-throughput technologies, and accumulation of various kinds of ‘-omics’ data in public repositories, there is an opportunity to retrieve, integrate, and reanalyze these resources to improve the diagnosis and treatment of different diseases and to provide mechanistic insights into host resistance in an efficient way. Meta-analysis is a relatively inexpensive option with good potential to increase the statistical power and generalizability of single-study analysis. In the current meta-analysis research, six microarray-based studies that investigate the transcriptome profile of mammary gland tissue after induced mastitis by E. coli infection were used. This meta-analysis not only reinforced the findings in individual studies, but also several novel terms including responses to hypoxia, response to drug, anti-apoptosis and positive regulation of transcription from RNA polymerase II promoter enriched by up-regulated genes. Finally, in order to identify the small sets of genes that are sufficiently informative in E. coli mastitis, the differentially expressed gene introduced by meta-analysis were prioritized by using ten different attribute weighting algorithms. Twelve meta-genes were detected by the majority of attribute weighting algorithms (with weight above 0.7) as most informative genes including CXCL8 (IL8), NFKBIZ, HP, ZC3H12A, PDE4B, CASP4, CXCL2, CCL20, GRO1(CXCL1), CFB, S100A9, and S100A8. Interestingly, the results have been demonstrated that all of these genes are the key genes in the immune response, inflammation or mastitis. The Decision tree models efficiently discovered the best combination of the meta-genes as bio-signature and confirmed that some of the top-ranked genes -ZC3H12A, CXCL2, GRO, CFB- as biomarkers for E. coli mastitis (with the accuracy 83% in average). This research properly indicated that by combination of two novel data mining tools, meta-analysis and machine learning, increased power to detect most informative genes that can help to improve the diagnosis and treatment strategies for E. coli associated with mastitis in cattle.

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“…NF-κB/p65 is the major transcription factor that regulates Cyclin D1 and Cyclin E1 transcription 21 , 22 . To investigate whether NF-κB pathway is involved in URGCP-increased Cyclin D1 and Cyclin E1 expression in glioma, we performed western blotting.…”

Section: Resultsmentioning

confidence: 99%

Downregulation of miR-16 via URGCP pathway contributes to glioma growth

Hong

Ouyang

Zhou³

et al. 2017

Sci Rep

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Experimental and clinical evidence points to a critical role of Upregulator of cell proliferation (URGCP/URG4) in controlling the progression of multiple tumors. However, the oncogenic role of URGCP in glioma still remains elusive. In this study we tried to investigate the oncogenic roles and molecular mechanisms of URGCP in glioma. We found that the levels of URGCP were upregulated in glioma, and that the high-levels of URGCP indicated a worse prognosis in glioma patients. URGCP and miR-16 are critical for glioma growth: silencing URGCP (shURGCP) inhibited glioma growth, while, the shURGCP-mediated proliferative inhibition could be recovered by antagonizing miR-16 (anta-miR-16) in vivo and in vitro. Mechanically, URGCP repressed miR-16 expression via activating NF-κB/c-myc pathway in glioma; Cyclins D1 and Cyclin E1 were identified as the direct targets of miR-16, thus, URGCP-mediated miR-16 downregulation accelerated cell proliferation by upregulating Cyclin D1 and Cyclin E1 expression. All these results suggested that URGCP accelerates glioma growth through the NF-κB/c-myc/miR-16/Cyclin D1/E1 pathway, and both URGCP and miR-16 function as a novel cell cycle regulators in glioma and could be considered as potential targets for glioma therapy.

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The involvement of nuclear factor-κappaB in the nuclear targeting and cyclin E1 upregulating activities of hepatoma upregulated protein

Cited by 13 publications

References 48 publications

Prognostic and predictive value of HURP in non‑small cell lung cancer

Prognostic and predictive value of HURP in non‑small cell lung cancer

Integration of machine learning and meta-analysis identifies the transcriptomic bio-signature of mastitis disease in cattle

Downregulation of miR-16 via URGCP pathway contributes to glioma growth

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