Evidence map›Paper›PMID 28498822›Full record

ArticleOncotarget2017

Interleukin-4 and interleukin-13 increase NADPH oxidase 1-related proliferation of human colon cancer cells.

Han Liu, Smitha Antony, Krishnendu Roy, Agnes Juhasz, Yongzhong Wu, Jiamo Lu, Jennifer L Meitzler, Guojian Jiang, Eric Polley, James H Doroshow

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

32 citing papers in PubMed, 50 citations in OpenAlex.

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  20. Inhibiting the Activity of NADPH Oxidase in Cancer.Antioxidants & redox signaling · 2020
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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

10 authors at 2 institutions in 1 country.

Han LiuDivision of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland, USA.
Smitha AntonyDivision of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland, USA.
Krishnendu RoyDivision of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland, USA.
Agnes JuhaszThe Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
Yongzhong WuThe Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
Jiamo LuThe Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
Jennifer L MeitzlerThe Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
Guojian JiangThe Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
Eric PolleyDivision of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland, USA.
James H DoroshowDivision of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland, USA.
Center for Cancer Research · USNational Cancer Institute · US

Funding

NADPH Oxidases as Novel Targets for Cancer TherapyZIABC010677 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DOROSHOW, JAMES · 2009 to 2025
$15.1M
6 · The paper itself

Abstract

Human colon cancers express higher levels of NADPH oxidase 1 [NOX1] than adjacent normal epithelium. It has been suggested that reactive oxygen species [ROS] derived from NOX1 contribute to DNA damage and neoplastic transformation in the colon, particularly during chronic inflammatory stress. However, the mechanism(s) underlying increased NOX1 expression in malignant tumors or chronic inflammatory states involving the intestine are poorly characterized. We examined the effects of two pro-inflammatory cytokines, IL-4 and IL-13, on the regulation of NOX1. NOX1 expression was increased 4- to 5-fold in a time- and concentration-dependent manner by both cytokines in human colon cancer cell lines when a functional Type II IL-4 receptor was present. Increased NOX1 transcription following IL-4/IL-13 exposure was mediated by JAK1/STAT6 signaling, was associated with a ROS-related inhibition of protein tyrosine phosphatase activity, and was dependent upon activation and specific binding of GATA3 to the NOX1 promoter. NOX1-mediated ROS production increased cell cycle progression through S-phase leading to a significant increase in cellular proliferation. Evaluation of twenty pairs of surgically-resected colon cancers and their associated uninvolved adjacent colonic epithelium demonstrated a significant increase in the active form of NOX1, NOX1-L, in tumors compared to normal tissues, and a significant correlation between the expression levels of NOX1 and the Type II IL-4 receptor in tumor and the uninvolved colon. These studies imply that NOX1 expression, mediated by IL-4/IL-13, could contribute to an oxidant milieu capable of supporting the initiation or progression of colonic cancer, suggesting a role for NOX1 as a therapeutic target.

Indexed as

Cell Line, TumorCell ProliferationColonic NeoplasmsHumansInterleukin-13Interleukin-4NADPH Oxidase 1Oxidative StressReactive Oxygen SpeciesIL13 protein, humanIL4 protein, humanInterleukin-13Interleukin-4NADPH Oxidase 1NOX1 protein, humanReactive Oxygen Speciescolon cancerinterleukin-13interleukin-4NADPH oxidasereactive oxygen species

Identifiers

PMID28498822
PMCPMC5503519
OpenAlexW2609567626

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.