Overexpression of interleukin-33 is associated with poor prognosis of patients with glioma

Zhang, Jian-Fei; Wang, Peng; Ji, Wei-yang; Ding, Yasuo; Lu, Xiao‐Jie

doi:10.1080/00207454.2016.1175441

Cited by 31 publications

(32 citation statements)

References 36 publications

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“…Recently, IL-33 was shown to be correlated with a bad prognosis in several types of cancer, although in some cases IL-33 behaves as a tumor suppressor by inducing an immune response. In terms of bad prognosis, high levels of IL-33 were detected in the serum and tumors of patients with glioma ( 56 ), gastric cancer ( 57 ), hepatocellular carcinoma ( 58 ), uterine leiomyoma ( 59 ), lung cancer ( 60 ), colorectal cancer ( 61 ), head and neck squamous cell carcinoma ( 62 ), and breast cancer ( 63 ), when compared to corresponding healthy tissues. The Cancer Genome Atlas Pan-Cancer analysis project showed and declared that the level of IL-33 expression is altered in only 3% of ~580 tumors and that the most common genetic alteration is the deletion of the IL-33 gene ( 64 ).…”

Section: Il-33 As a Marker For Good Or Poor Prognosismentioning

confidence: 99%

Section: Il-33 As a Marker For Good Or Poor Prognosismentioning

confidence: 99%

“…Lu and collaborators detected “significantly higher IL-33 expression in glioma tissues than in normal brain tissues through immune-histochemical (IHC) analysis” ( 56 ). High IL-33 expression in glioma was correlated with shorter overall survival (OS) and progression-free survival (PFS) ( 56 ). In women, IL-33 highly promotes epithelial cell proliferation and tumorigenesis in breast cancer, since IL-33 increases Cancer Osaka Thyroid (COT) phosphorylation via ST2-COT interaction in normal epithelial and breast cancer cells.…”

Section: Il-33 As a Marker For Good Or Poor Prognosismentioning

confidence: 99%

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The Pro-tumorigenic IL-33 Involved in Antitumor Immunity: A Yin and Yang Cytokine

Fournié

Poupot

2018

Front. Immunol.

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Interleukin-33 (IL-33), considered as an alarmin released upon tissue stress or damage, is a member of the IL-1 family and binds the ST2 receptor. First described as a potent initiator of type 2 immune responses through the activation of T helper 2 (TH2) cells and mast cells, IL-33 is now also known as an effective stimulator of TH1 immune cells, natural killer (NK) cells, iNKT cells, and CD8 T lymphocytes. Moreover, IL-33 was shown to play an important role in several cancers due to its pro and anti-tumorigenic functions. Currently, IL-33 is a possible inducer and prognostic marker of cancer development with a direct effect on tumor cells promoting tumorigenesis, proliferation, survival, and metastasis. IL-33 also promotes tumor growth and metastasis by remodeling the tumor microenvironment (TME) and inducing angiogenesis. IL-33 favors tumor progression through the immune system by inducing M2 macrophage polarization and tumor infiltration, and upon activation of immunosuppressive cells such as myeloid-derived suppressor cells (MDSC) or regulatory T cells. The anti-tumor functions of IL-33 also depend on infiltrated immune cells displaying TH1 responses. This review therefore summarizes the dual role of this cytokine in cancer and suggests that new proposals for IL-33-based cancer immunotherapies should be considered with caution.

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Section: Il-33 As a Marker For Good Or Poor Prognosismentioning

confidence: 99%

Section: Il-33 As a Marker For Good Or Poor Prognosismentioning

confidence: 99%

Section: Il-33 As a Marker For Good Or Poor Prognosismentioning

confidence: 99%

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The Pro-tumorigenic IL-33 Involved in Antitumor Immunity: A Yin and Yang Cytokine

Fournié

Poupot

2018

Front. Immunol.

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“…More recently, it was reported that IL-33 is highly expressed in glioma cells and facilitates cell proliferation and migration via the regulation of growth factor and chemokine expression ( 24 ). Previously, we detected the overexpression of IL-33 in glioma tissues compared with that in normal brain tissues, and identified IL-33 overexpression as an independent factor that predicted a poor prognosis in patients with glioma ( 25 ). However, the underlying molecular mechanisms of the IL-33/ST2 axis during glioma development remain to be elucidated.…”

Section: Introductionmentioning

confidence: 97%

IL-33 enhances glioma cell migration and invasion by upregulation of MMP2 and MMP9 via the ST2-NF-κB pathway

et al. 2017

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As an important member of the interleukin (IL)-1 family, IL-33 plays a significant role in tumor progression. To explore this, we previously analyzed the association between IL-33 expression and the prognosis of patients with glioma. However, the function of the IL-33/ST2 axis in glioma remained unclear. In the present study, immunofluorescent staining results revealed that the expression levels of IL-33 and ST2 receptor in glioma tissues were higher than those in normal brain tissues. Invasion and migration assays demonstrated that IL-33 significantly increased glioma cell invasion and migration in vitro. Furthermore, knockdown of ST2 by siRNA attenuated the IL-33-induced increase in invasion and migration. In addition, ELISA results revealed that IL-33 upregulated the expression of matrix metalloproteinase (MMP)2 and MMP9. Western blot analysis results indicated that IL-33 stimulation increased the phosphorylation of nuclear factor-κB (NF-κB) in a time- and dose-dependent manner. Moreover, silencing of the NF-κB pathway by BAY 11–7082 resulted in the inhibition of IL-33-induced invasion and migration, as well as the downregulation of MMP2 and MMP9 production. These findings indicate that IL-33 may be involved in the process of glioma cell invasion and migration by upregulating MMP2 and MMP9 via the ST2-NF-κB signaling pathway. Thus, IL-33 may be a novel therapeutic target for glioma.

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“…Pullen et al myeloid granulocytes have gained attention in other areas, especially due to proven alternative, IgE-independent activation schemes, notably through IL33/ST2, and for their potent nociceptive effects on the somatosensory system (though mechanistic details are scant). A timely review of mast cells in neuroinflammation is explained by Skaper et al 180 Astrocytes are known to activate microglia through IL33, 181 and furthermore there are reports linking IL33 induction with decreased survival time 182 and IL33 stimulating expression of MMP2 and MMP9 from immortal cell cultures. 183 Of note is that IL33 positively regulates mast-cell survival and inflammatory functions, [184][185][186] and thus it will be important to investigate a potential pathological link between gliomas and mast cells via IL33 signaling.…”

mentioning

confidence: 99%

Current insights into matrix metalloproteinases and glioma progression: transcending the degradation boundary

Pullen¹,

Pickford²,

Perry³

et al. 2018

MNM

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Glioblastoma multiforme (GBM) remains one of the most deadly cancers, with modest advances in overall survival despite significant improvements in imaging, surgery, and molecular genomic understanding. The highest-grade glioma, GBM is a primary brain cancer that is molecularly heterogeneous among patients and even within the same patient. Key hallmarks include glioma-cell invasion, angiogenesis, and therapeutic resistance. While once considered a major player in glioma invasion, members of the MMP family are also associated with other key pathological hallmarks of glioma. Investigations into understanding MMP function in GBM were slowed due to the failed MMP-inhibitor trials for GBM in the 2000s. In contrast, the field of MMPs in other brain pathologies has flourished in such areas as traumatic brain injury, multiple sclerosis, and stroke. In the past decade, the increase in publicly available data sets documenting patient-biopsy molecular information has empowered laboratory investigations into the spectrum of genomic, transcriptomic, and proteomic changes associated with glioma, including MMPs. In this review, we selected one of these data sets to illustrate a small sample of information that can be obtained from such analyses. Combined with recent reports on the use of MMP-cleavable peptides for imaging and the multifunctionality of MMPs, including intracellular nonproteolytic actions in various cell types, this paves the way for new avenues of MMP research. Understanding the function of MMPs in host-tumor interactions both spatially and temporally during tumor progression and in response to treatment will be crucial for the advancement of targeting specific MMPs in GBM. The opportunities to explore MMP regulation, expression, and function further in GBM have never been so great with progress in modern bioinformatics and molecular techniques, and it is hoped that advancements will translate in some way to patients diagnosed with GBM.

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Overexpression of interleukin-33 is associated with poor prognosis of patients with glioma

Cited by 31 publications

References 36 publications

The Pro-tumorigenic IL-33 Involved in Antitumor Immunity: A Yin and Yang Cytokine

The Pro-tumorigenic IL-33 Involved in Antitumor Immunity: A Yin and Yang Cytokine

IL-33 enhances glioma cell migration and invasion by upregulation of MMP2 and MMP9 via the ST2-NF-κB pathway

Current insights into matrix metalloproteinases and glioma progression: transcending the degradation boundary

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