Cellular and clinicopathological features of the IL-33/ST2 axis in human esophageal squamous cell carcinomas

Cui, Guanglin; Ren, Jingli; Xu, Gang; Li, Zhenfeng; Zheng, Wei; Yuan, Ang

doi:10.1186/s12935-018-0700-2

Cited by 13 publications

(14 citation statements)

References 60 publications

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“…Studies on several malignancies (including renal cancer) suggest that the IL33/IL33Rα axis could be important in tumorigenesis through exerting direct effects on malignant cells [ 64 ] or indirectly through effects on stromal cells [ 65 ], including altering the regulation of tumor angiogenesis [ 66 ]. An association between serum IL33Rα levels and prognosis has been described for patients with hepatocellular carcinoma [ 67 ] and breast cancer [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

The Biological Context of C-Reactive Protein as a Prognostic Marker in Renal Cell Carcinoma: Studies on the Acute Phase Cytokine Profile

Aarstad

Guðbrandsdottir

Hjelle

et al. 2020

Cancers

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High serum levels of the acute phase protein C-reactive protein (CRP) are associated with an adverse prognosis in renal cancer. The acute phase reaction is cytokine-driven and includes a wide range of inflammatory mediators. This overall profile of the response depends on the inducing event and can also differ between patients. We investigated an extended acute phase cytokine profile for 97 renal cancer patients. Initial studies showed that the serum CRP levels had an expected prognostic association together with tumor size, stage, nuclear grading, and Leibovich score. Interleukin (IL)6 family cytokines, IL1 subfamily mediators, and tumor necrosis factor (TNF)α can all be drivers of the acute phase response. Initial studies suggested that serum IL33Rα (the soluble IL33 receptor α chain) levels were also associated with prognosis, although the impact of IL33Rα is dependent on the overall cytokine profile, including seven IL6 family members (IL6, IL6Rα, gp130, IL27, IL31, CNTF, and OSM), two IL1 subfamily members (IL1RA and IL33Rα), and TNFα. We identified a patient subset characterized by particularly high levels of IL6, IL33Rα, and TNFα alongside an adverse prognosis. Thus, the acute phase cytokine reaction differs between renal cancer patients, and differences in the acute phase cytokine profile are associated with prognosis.

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Section: Discussionmentioning

confidence: 99%

The Biological Context of C-Reactive Protein as a Prognostic Marker in Renal Cell Carcinoma: Studies on the Acute Phase Cytokine Profile

Aarstad

Guðbrandsdottir

Hjelle

et al. 2020

Cancers

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“…Hollande et al found that IL‐33 was essential and active for eosinophil‐mediated antitumor responses. Cui et al observed that the IL‐33/ST2 axis might be involved in the progression of human ESCC. However, the molecular mechanism of IL‐33 in ESCC development remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Interleukin‐33‐nuclear factor‐κB‐CCL2 signaling pathway promotes progression of esophageal squamous cell carcinoma by directing regulatory T cells

Lian

Luo

et al. 2020

Cancer Science

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Esophageal cancer is currently one of the most fatal cancers. However, there is no effective treatment. Increasing evidence suggests that interleukin (IL)‐33 has a significant role in tumor progression and metastasis. Currently, the underlying cellular and molecular mechanism of IL‐33 in promoting esophageal squamous cell carcinoma (ESCC) remains unclear. In this study, we investigated whether IL‐33 could induce the epithelial‐mesenchymal transition (EMT) in ESCC. Interleukin‐33 expression was examined in ESCC and corresponding adjacent normal tissues by immunohistochemistry and quantitative real‐time PCR experiments. Elevated IL‐33 levels were observed in ESCC tissues. Further in vitro experiments were undertaken to elucidate the effect of IL‐33 on migration and invasion in KYSE‐450 and Eca‐109 esophageal cancer cells. Knockdown of IL‐33 decreased the metastasis and invasion capacity in esophageal cancer cells, whereas IL‐33 overexpression showed the opposite effect. We then screened CCL2 which is a downstream molecule of IL‐33, and proved that IL‐33 could promote tumor development and metastasis by recruiting regulatory T cells (Tregs) through CCL2, and IL‐33 regulated the expression of CCL2 through transforming growth factor‐β in Treg cells. Knockdown of IL‐33 decreased the development of human ESCC xenografts in BALB/c nude mice. Collectively, we found that the IL‐33/nuclear factor‐κB/CCL2 pathway played an essential role in human ESCC progress. Hence, IL‐33 should be considered as an effective therapy target for ESCC.

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“…IL-33/ST2 axis was involved in the activity of mast cells during colitis, and IL-33 promoted the percentage of IL-13/IL-22 producing T cells, which indicated that IL-33 regulated T cell differentiation and function [24]. In addition, IL-33/ST2 axis was involved in the proliferation of ESCC cells and stromal cells, and the IL-33 or ST2 positive cells in ESCC stroma were positively related to node involvement, invasion depth and TNM stage [25]. Importantly, IL-33/ST2 axis was involved in the regulation of myocardial cell apoptosis [5,6].…”

Section: Discussionmentioning

confidence: 92%

LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2

Yang

Huang

et al. 2019

Cell Cycle

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Objective: To investigate the role of lncRNA ANRIL in the modulation of myocardial cell apoptosis in acute myocardial infarction (AMI). Methods: AMI mice model was established, and lncRNA ANRIL, IL-33 and ST2 expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The apoptosis of myocardial cells was detected by TUNEL assay. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between lncRNA ANRIL and USP17. Results: Compared with sham group, lncRNA ANRIL and ST2 expression levels were up-regulated, and the apoptosis of myocardial cells was increased in heart tissues of AMI group. Compared with normoxia group, the apoptosis of mouse myocardial cell HL-1 and primary murine myocardial cells was increased, and lncRNA ANRIL and ST2 expression levels were up-regulated in hypoxia group. We also found up-regulation of IL-33 in AMI group and hypoxia group. Besides, lncRNA ANRIL affected deubiquitinase USP17-mediated degradation of IL-33. Interfering lncRNA ANRIL reduced the apoptosis of myocardial cells through IL-33/ST2 pathway. In vivo experiments found that interfering lncRNA ANRIL relieved myocardial cell apoptosis and improved heart function in AMI mice. Conclusion: LncRNA ANRIL regulated myocardial cell apoptosis through IL-33/ST2 pathway.

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Cellular and clinicopathological features of the IL-33/ST2 axis in human esophageal squamous cell carcinomas

Cited by 13 publications

References 60 publications

The Biological Context of C-Reactive Protein as a Prognostic Marker in Renal Cell Carcinoma: Studies on the Acute Phase Cytokine Profile

The Biological Context of C-Reactive Protein as a Prognostic Marker in Renal Cell Carcinoma: Studies on the Acute Phase Cytokine Profile

Interleukin‐33‐nuclear factor‐κB‐CCL2 signaling pathway promotes progression of esophageal squamous cell carcinoma by directing regulatory T cells

LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2

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