Evidence map›Paper›PMID 28330870›Full record

ArticleThe Journal of biological chemistry2017

Nuclear factor erythroid 2-related factor 2 enhances carcinogenesis by suppressing apoptosis and promoting autophagy in nickel-transformed cells.

Young-Ok Son, Poyil Pratheeshkumar, Sasidharan Padmaja Divya, Zhuo Zhang, Xianglin Shi

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  9. Dual Roles of Oxidative Stress in Metal Carcinogenesis.Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer · 2017
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Young-Ok SonCenter for Research on Environmental Disease; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536-0305; National Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 61005, South Korea. Electronic address: sounagi@gist.ac.kr.
Poyil PratheeshkumarCenter for Research on Environmental Disease; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536-0305.
Sasidharan Padmaja DivyaDepartment of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536-0305.
Zhuo ZhangDepartment of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536-0305.
Xianglin ShiCenter for Research on Environmental Disease; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536-0305. Electronic address: xshi5@email.uky.edu.
University of Kentucky · USGwangju Institute of Science and Technology · KR

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Mechanisms of As-Induced CarcinogenesisR01CA119028 · NCI · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2006 to 2010
$1.8M
Apple Peel Extract Protects UV-Induced CarcinogenesisR01ES015375 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2006 to 2010
$1.7M
Reactive oxygen species in Ni(II) carcinogenesisR01ES015518 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2008 to 2012
$1.6M
Oxidative Stress in Cr(VI)-induced CarcinogenesisR01CA116697 · NCI · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2007 to 2011
$1.4M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA116697NCI NIH HHS R01 CA119028NIEHS NIH HHS R01 ES015375NIEHS NIH HHS R01 ES015518
6 · The paper itself

Abstract

Nickel-containing compounds are widely used in industry. Nickel is a known human carcinogen that primarily affects the lungs. Proposed mechanisms of nickel-induced carcinogenesis include disruption of cellular iron homeostasis, generation of reactive oxygen species (ROS), and induction of hypoxia signaling. However, the precise molecular mechanisms of nickel-induced malignant transformation and tumor development remain unclear. This study shows that the transcription factor Nrf2 is highly expressed in lung tumor tissue and in nickel-transformed human lung bronchial epithelial BEAS-2B cells (NiT cells). Additionally, constitutively high levels of Nrf2 play a critical role in apoptosis resistance in NiT cells. Basal ROS levels were extremely low in NiT cells and were correlated with elevated expression levels of both antioxidant enzymes (

Indexed as

ApoptosisAutophagybcl-X ProteinCatalaseCell Line, TransformedCell Transformation, NeoplasticGene Knockdown TechniquesHumansNF-E2-Related Factor 2NickelProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSignal TransductionSTAT3 Transcription FactorSuperoxide DismutaseBCL2L1 protein, humanBCL2 protein, humanbcl-X ProteinCatalaseNFE2L2 protein, humanNF-E2-Related Factor 2NickelProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSTAT3 protein, humanSTAT3 Transcription FactorSuperoxide Dismutaseapoptosisautophagycarcinogenesisnickelnuclear factor 2 (erythroid-derived 2-like factor) (NFE2L2) (Nrf2)transformed cells

Identifiers

PMID28330870
PMCPMC5437238
OpenAlexW2598008721

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.