The Association of Serum IL-33 and sST2 with Breast Cancer

Yang, Zhiping; Ling, Dan-yan; Xie, Youhua; Wu, Wanxin; Li, Jingrui; Jin, Jianhua; Ji, Zheng; Fan, Yun; Zhang, Ye

doi:10.1155/2015/516895

Cited by 52 publications

(53 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In line with previous findings in other cancers, like myeloproliferative disorders, hepatic cancer, and breast cancer, we found increased serum concentrations of ST2 in MF. Moreover, ST2 concentrations were significantly higher in more advanced stages of MF.…”

Section: Discussionsupporting

confidence: 92%

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

et al. 2019

View full text Add to dashboard Cite

Background Mycosis fungoides (MF) skin lesions are characterized by low-grade inflammation, which may be sustained by proinflammatory cytokines as probably interleukin-33 (IL-33). We compared serum concentrations of IL-33 and its receptor ST2 and the frequency of selected IL-33 single nucleotide polymorphisms (SNPs) between patients with MF and healthy controls.Methods In 88 patients with MF and 66 healthy controls, we analyzed SNPs in the 9894 and 11877 loci of the IL-33 gene. Moreover, we measured serum concentrations of IL-33 and its receptor ST2.Results There were no statistically significant differences in the frequencies of both IL-33 SNPs between patients and controls. Compared with controls, patients with MF had similar IL-33 serum concentrations (P = 0.71) but significantly increased ST2 concentrations (P < 0.001). Patients in MF-IA stage had significantly lower ST2 serum concentrations than those with the remaining MF stages (P = 0.002). The studied variables were not related to pruritus severity. Patients with the C(+) IL-33 11877 SNP had lower ST2 serum concentrations than patients with the C(À) 11877 SNP (P = 0.043).Conclusions It was published before that the knockout of the ST2 gene after injection of IL-33 is associated with a reduced inflammatory reaction in the skin, as well as that IL-33 plays a role in allergic and neoplastic disorders. Concerning the difference in ST2 concentration between control and MF group, and C IL-33 11877 SNP possibly influencing the ST2 concentration, the role of IL-33/ST2 signaling, needs further studies.

show abstract

Section: Discussionsupporting

confidence: 92%

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In breast cancer patients, serum levels of IL-33 and of its decoy receptor sST2 were enhanced compared to healthy controls. This positively correlated with the expression of vascular endothelial growth factor (VEGF), metalloprotease-11 (MMP-11), or platelet-derived growth factor-C, which are markers of poor prognosis in breast cancer (52). …”

Section: Main Review Textmentioning

confidence: 99%

“…For breast cancer, IL-33 and sST2 may also serve as non-invasive diagnostic marker, as these two proteins are upregulated in the serum of patients [(52) and see also the paragraph on breast cancer above]. However, IL-33 is upregulated in different types of inflammatory diseases (114–116) and cancers (111, 112), and this lack of specificity may prevent its use as a biomarker in the daily clinic diagnostic.…”

Section: Main Review Textmentioning

confidence: 99%

The Role of IL-33-Dependent Inflammation in the Tumor Microenvironment

Wasmer

Krebs

2017

Front. Immunol.

View full text Add to dashboard Cite

There is compelling evidence that inflammation contributes to tumorigenesis. Inflammatory mediators within the tumor microenvironment can either promote an antitumor immune response or support tumor pathogenesis. Therefore, it is critical to determine the relative contribution of tumor-associated inflammatory pathways to cancer development. Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that is released upon tissue stress or damage to operate as an alarmin. IL-33 has been primarily implicated in the induction of type-2 immune responses. However, recent findings have shown a role of IL-33 in several cancers where it may exert multiple functions. In this review, we will present the current knowledge on the role of IL-33 in the microenvironment of different tumors. We will highlight which cells produce and which cells are activated by IL-33 in cancer. Furthermore, we will explain how IL-33 modulates the tumor-associated inflammatory microenvironment to restrain or promote tumorigenesis. Finally, we will discuss the issues to be addressed first before potentially targeting the IL-33 pathway for cancer therapy.

show abstract

“…IL-33 has been found to mediate Th2 immune responses by binding and signaling through ST2L, an orphan receptor in the IL-1R family, to induce NF-κB and MAPK (p38, JNK and ERK1/2) activation, and promote Th2 cytokine production [19][20][21][22][23]. Recent studies have revealed that IL-33 plays a functional role in tumor development, with high levels of serum IL-33 associated with poor prognosis and chemotherapy resistance in various cancers [24][25][26][27][28][29][30]. An IL-33-dependent proliferation response can be induced by the increase and recruitment of type 2 innate lymphoid cells (ILC2s) [31], which produce high levels of IL-13 that consequently promote cholangiocyte hyperplasia [32].…”

Section: Introductionmentioning

confidence: 99%

The reciprocal interaction between tumor cells and activated fibroblasts mediated by TNF-α/IL-33/ST2L signaling promotes gastric cancer metastasis

et al. 2019

View full text Add to dashboard Cite

Gastric cancer (GC) is characterized by extensive local invasion, distant metastasis and poor prognosis. In most cases, GC progression is associated with aberrant expression of cytokines or activation of signaling cascades mediated by tumor-stroma interactions. However, the mechanisms by which these interactions contribute to GC progression are poorly understood. In this study, we find that IL-33 and its receptor ST2L are upregulated in the human GC and served as prognostic markers for poor survival of GC patients. In a co-culture model with GC cells and cancer-associated fibroblasts (CAFs), we further demonstrate that CAFs-derived IL-33 enhances the migration and invasion of GC cells by inducing the epithelial-mesenchymal transition (EMT) through activation of the ERK1/2-SP1-ZEB2 pathway in a ST2L-dependent manner. Furthermore, the secretion of IL-33 by CAFs can be induced by the proinflammatory cytokines TNF-α that is released by GC cells via TNFR2-NF-κB-IRF-1 pathway. Additionally, silencing of IL-33 expression in CAFs or ST2L expression in GC cells inhibits the peritoneal dissemination and metastatic potential of GC cells in nude mice. Taken together, these results characterize a critical role of the interaction between epithelial-stroma mediated by the TNF-α/IL-33/ ST2L signaling in GC progression, and provide a rationale for targeting this pathway to treat GC metastasis.

show abstract

The Association of Serum IL-33 and sST2 with Breast Cancer

Cited by 52 publications

References 21 publications

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

The Role of IL-33-Dependent Inflammation in the Tumor Microenvironment

The reciprocal interaction between tumor cells and activated fibroblasts mediated by TNF-α/IL-33/ST2L signaling promotes gastric cancer metastasis

Contact Info

Product

Resources

About