Nuclear unphosphorylated STAT3 correlates with a worse prognosis in human glioblastoma

Rodrigues, Bruna R.; Queiroz‐Hazarbassanov, Nicolle; Lopes, Marilene H.; Bleggi-Torres, L. F.; Suzuki, Sergio Hideki; Cunha, Isabela Werneck da; Sanematsu, Paulo; Martins, Vilma R.

doi:10.1016/j.prp.2016.03.001

Cited by 13 publications

(13 citation statements)

References 27 publications

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“…Moreover, the U-STAT3/NF-κB complex appears to activate NF-κB-regulated genes in B-cell neoplasms, and contributes to pathogenesis of those cells as well [ 61 ]. These observations are also consistent with another report demonstrating that nuclear U-STAT3 accumulation correlates with a poor prognosis for human glioblastoma [ 62 ], suggesting an important role of U-STAT3 in oncogenesis [ 63 ]. For IFN-mediated signaling, a recent study suggested that U-STAT3 plays an important role in the IFNs response pathway and showed that 60% of interferon-stimulated genes are STAT3-dependent and 30% are independent of STAT3 tyrosine phosphorylation [ 49 ].…”

Section: Canonical and Non-canonical Jak/stat Activationsupporting

confidence: 93%

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Nan

Zhang

2018

Viruses

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Interferons (IFNs) are a group of secreted proteins that play critical roles in antiviral immunity, antitumor activity, activation of cytotoxic T cells, and modulation of host immune responses. IFNs are cytokines, and bind receptors on cell surfaces to trigger signal transduction. The major signaling pathway activated by IFNs is the JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway, a complex pathway involved in both viral and host survival strategies. On the one hand, viruses have evolved strategies to escape from antiviral host defenses evoked by IFN-activated JAK/STAT signaling. On the other hand, viruses have also evolved to exploit the JAK/STAT pathway to evoke activation of certain STATs that somehow promote viral pathogenesis. In this review, recent progress in our understanding of the virus-induced IFN-independent STAT signaling and its potential roles in viral induced inflammation and pathogenesis are summarized in detail, and perspectives are provided.

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Section: Canonical and Non-canonical Jak/stat Activationsupporting

confidence: 93%

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Nan

Zhang

2018

Viruses

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“…Balaram et al also found that STAT1 is upregulated in GBM and correlated with a worse prognosis [28]. Another study suggested STAT3 as a potential biomarker for the prognosis of GBM [29]. Therefore, we suggested that STAT family may act as potential prognostic biomarkers in GBM.…”

Section: Discussionsupporting

confidence: 56%

Identification of therapeutic targets and prognostic biomarkers among STAT family in glioblastoma

Li¹,

Zhou²,

Deng³

et al. 2020

Preprint

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Background: Glioblastoma (GBM) is the most common and aggressive primary brain malignancies with high incidence and mortality. The aberrant activation of STAT signaling was confirmed to result in tumor pathogenesis and progress by regulating cell cycle, cell survival, and immune response. Methods: The clinical significance of and regulation network of STAT family in GBM were explored with several web applications or database. Results: The level of STAT1/3/5A/5B/6 were increased in GBM while STAT4 level was decreased. GBM patients with high expression of STAT1/2/3/5A/6 and low expression of STAT4/5B had a worse overall survival. Among the STAT family, STAT 4 and STAT6 were the top two frequently mutated genes. Correlation suggested a low to moderate correlation among STAT family. STAT family were also involved in the activation or inhibition of the famous cancer related pathways. Immune infiltrates analysis suggested that STAT5A level showed significantly correlated with the abundance of immune cells and the level of immune gene biomarkers. GO functions and KEGG pathways analysis revealed that STAT5A was involved in immune response-regulating signaling pathway, neutrophil and lymphocyte mediated immunity, single-stranded DNA binding, cytokine-cytokine receptor interaction, NOD-like receptor signaling pathway, NF-kappa B signaling pathway, and TNF signaling pathway. Moreover, we also identified several Kinase and transcription factor targets of STAT5A in GBM. Conclusions: Our results revealed the therapeutic targets, prognostic biomarkers and regulation network of STAT family in GBM, laying the foundation for further studies about STAT family in therapy and prognosis of GBM.

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“…Additionally, un-phosphorylated STAT3 is also thought to be involved in transcriptional regulation, being able to translocate to the nucleus, bind DNA both directly and indirectly, and activate transcription of target genes including several oncogenes [37][38][39]. Indeed, high levels of nuclear un-phosphorylated STAT3 correlate with a bad prognosis in glioblastoma [40].…”

Section: Tyrosine Phosphorylationmentioning

confidence: 99%

STAT3 in cancer: A double edged sword

et al. 2017

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The transcription factor signal transducer and activator of transcription (STAT) 3 is activated downstream of cytokines, growth factors and oncogenes to mediate their functions under both physiological and pathological conditions. In particular, aberrant/unrestrained STAT3 activity is detected in a wide variety of tumors, driving multiple pro-oncogenic functions. For that, STAT3 is widely considered as an oncogene and is the object of intense translational studies. One of the distinctive features of this factor is however, its ability to elicit different and sometimes contrasting effects under different conditions. In particular, STAT3 activities have been shown to be either pro-oncogenic or tumor-suppressive according to the tumor aetiology/mutational landscape, suggesting that the molecular bases underlining its functions are still incompletely understood. Here we discuss some of the properties that may provide the bases to explain STAT3 heterogeneous functions, and in particular how post-translational modifications contribute shaping its sub-cellular localization and activities, the cross talk between these activities and cell metabolic conditions, and finally how its functions can control the behaviour of both tumor and tumor microenvironment cell populations.

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Nuclear unphosphorylated STAT3 correlates with a worse prognosis in human glioblastoma

Cited by 13 publications

References 27 publications

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

Identification of therapeutic targets and prognostic biomarkers among STAT family in glioblastoma

STAT3 in cancer: A double edged sword

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