Evidence map›Paper›PMID 29662196›Full record

ArticleOncogene2018

Tocopherols inhibit esophageal carcinogenesis through attenuating NF-κB activation and CXCR3-mediated inflammation.

Hui Yang, Miao Xu, Fang Lu, Qiannan Zhang, Yongquan Feng, Chung S Yang, Ning Li, Xudong Jia

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  3. Tumorous IRE1α facilitates CD8Cell communication and signaling : CCS · 2024
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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 4 institutions in 2 countries.

Hui YangKey Laboratory of Food Safety Risk Assessment of Ministry of Health, National Center for Food Safety Risk Assessment, Beijing, China. yanghui@cfsa.net.cn.
Miao XuWest China School of Public Health, Sichuan University, Chengdu, China.
Fang LuBeijing University of Agriculture, Beijing, China.
Qiannan ZhangKey Laboratory of Food Safety Risk Assessment of Ministry of Health, National Center for Food Safety Risk Assessment, Beijing, China.
Yongquan FengKey Laboratory of Food Safety Risk Assessment of Ministry of Health, National Center for Food Safety Risk Assessment, Beijing, China.
Chung S YangDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Ning LiKey Laboratory of Food Safety Risk Assessment of Ministry of Health, National Center for Food Safety Risk Assessment, Beijing, China.
Xudong JiaKey Laboratory of Food Safety Risk Assessment of Ministry of Health, National Center for Food Safety Risk Assessment, Beijing, China. jiaxudong@cfsa.net.cn.ORCID http://orcid.org/0000-0002-6025-338X
China National Center for Food Safety Risk Assessment · CNBeijing University of Agriculture · CNRutgers, The State University of New Jersey · USSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer is one of the common causes of cancer mortality in the world. The predominant histological subtype, esophageal squamous cell carcinoma (ESCC), often results in poor prognosis due to the lack of effective approaches for the early diagnosis and treatment, highlighting the need for preventive intervention against this disease. Here we report that dietary tocopherols significantly prevents esophageal carcinogenesis by inhibiting the activation of NF-κB and the subsequent interaction of chemokine CXCL9/10/11 with their receptor CXCR3 in ESCC induced by N-nitrosomethylbenzylamine (NMBA) in murine models. Dietary supplementation with 0.15% α-tocopherol (α-T), δ-tocopherol (δ-T), or γ-tocopherol rich mixture (γ-TmT) markedly suppressed the production of pro-inflammatory cytokines, as well as the induction of CXCR3+ effector T cells (CD4+ Th1 and CD8+ CTLs) infiltration, especially at the early stage of carcinogenesis. In experiments in vivo and in vitro, these events were tightly correlated with the blockade of NF-κB activation. Our results show that tocopherols decrease carcinogenesis through inhibiting NF-κB and CXCR3 signaling, as well as related inflammation in early premalignant lesions. This pathway may offer a novel target for chemoprevention of esophageal cancer.

Indexed as

AnimalsCarcinogenesisEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansInflammationInflammation MediatorsMaleMiceMice, Inbred C57BLNF-kappa BRats, Inbred F344Receptors, CXCR3Signal TransductionT-LymphocytesTocopherolsInflammation MediatorsNF-kappa BReceptors, CXCR3Tocopherols

Identifiers

PMID29662196
OpenAlexW2800610194

What OpenQuestion holds

Textmetadata
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.