Evidence map›Paper›PMID 31883400›Full record

ArticleCancer science2020

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

Ying Yue, Jingyao Lian, Tian Wang, Chenghan Luo, Yiqiang Yuan, Guohui Qin, Bin Zhang, Yi Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

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  4. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Ying YueBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jingyao LianBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Tian WangBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chenghan LuoBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yiqiang YuanClinical Laboratory, The Seventh People's Hospital of Zhengzhou, Zhengzhou, China.
Guohui QinBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Bin ZhangDepartment of Hematology/Oncology, School of Medicine, Northwestern University, Chicago, IL, USA.
Yi ZhangBiotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID https://orcid.org/0000-0001-9861-4681
First Affiliated Hospital of Zhengzhou University · CNHenan Cancer Hospital · CNNorthwestern University · US

Funding

National Natural Science Foundation of China U1804281
6 · The paper itself

Abstract

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.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationChemokine CCL2Disease ProgressionEpithelial-Mesenchymal TransitionEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticHumansInterleukin-33MiceMice, Inbred BALB CMice, NudeCCL2 protein, humanChemokine CCL2IL33 protein, humanInterleukin-33NF-kappa BCCL2esophageal squamous cell carcinomaIL-33NF-κBTreg

Identifiers

PMID31883400
PMCPMC7060484
OpenAlexW2997748108

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.