Evidence map›Paper›PMID 27470422›Full record

ArticleToxicology and applied pharmacology2016

Different roles of ROS and Nrf2 in Cr(VI)-induced inflammatory responses in normal and Cr(VI)-transformed cells.

Ram Vinod Roy, Poyil Pratheeshkumar, Yong-Ok Son, Lei Wang, John Andrew Hitron, Sasidharan Padmaja Divya, Zhuo Zhang, Xianglin Shi

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Nrf2/cyclooxygenase 2 signaling in Cr(VI)-induced carcinogenesis.Ecotoxicology and environmental safety · 2025
    Article
  3. Lignans: Advances in Biosynthesis, Bioavailability, and Pharmacological Activity.Combinatorial chemistry & high throughput screening · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Optimization extraction and bioactivities of polysaccharide from wildSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2017
    Article
  13. 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
  14. Article
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 1 institution in 1 country.

Ram Vinod RoyCenter for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
Poyil PratheeshkumarCenter for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
Yong-Ok SonCenter for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
Lei WangCenter for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
John Andrew HitronCenter for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
Sasidharan Padmaja DivyaDepartment of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
Zhuo ZhangDepartment of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA.
Xianglin ShiCenter for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA. Electronic address: xshi5@email.uky.edu.
University of Kentucky · US

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
TRAINING GRANT IN MOLECULAR MECHANISMS OF TOXICITY.T32ES007266 · NIEHS · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI, MELLON, ISABEL W · 1990 to 2020
$3.7M
Prevention of UV-induced carcinogenesis by cyanidin-3-glucosideR01ES017244 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2011 to 2015
$1.7M
Cell survival and arsenic carcinogenesisR01ES020870 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2012 to 2016
$1.7M
Reactive oxygen species in Ni(II) carcinogenesisR01ES015518 · NIEHS · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2008 to 2012
$1.6M
NCI NIH HHS P30 CA177558NIEHS NIH HHS R01 ES015518NIEHS NIH HHS R01 ES017244NIEHS NIH HHS R01 ES020870NIEHS NIH HHS T32 ES007266
6 · The paper itself

Abstract

Hexavalent chromium (Cr(VI)) is classified as a human carcinogen. Cr(VI) has been associated with adenocarcinomas and squamous cell carcinoma of the lung. The present study shows that acute Cr(VI) treatment in human bronchial epithelial cells (BEAS-2B) increased inflammatory responses (TNF-α, COX-2, and NF-кB/p65) and expression of Nrf2. Cr(VI)-induced generation of reactive oxygen species (ROS) are responsible for increased inflammation. Despite the fact that Nrf2 is a master regulator of response to oxidative stress, silencing of Nrf2 in the acute Cr(VI) treatment had no effect on Cr(VI)-induced inflammation. In contrast, in Cr(VI)-transformed (CrT) cells, Nrf2 is constitutively activated. Knock-down of this protein resulted in decreased inflammation, while silencing of SOD2 and CAT had no effect in the expression of these inflammatory proteins. Results obtained from the knock-down of Nrf2 in CrT cells are very different from the results obtained in the acute Cr(VI) treatment. In BEAS-2B cells, knock-down of Nrf2 had no effect in the inflammation levels, while in CrT cells a decrease in the expression of inflammation markers was observed. These results indicate that before transformation, ROS plays a critical role while Nrf2 not in Cr(VI)-induced inflammation, whereas after transformation (CrT cells), Nrf2 is constitutively activated and this protein maintains inflammation while ROS not. Constitutively high levels of Nrf2 in CrT binds to the promoter regions of COX-2 and TNF-α, leading to increased inflammation. Collectively, our results demonstrate that before cell transformation ROS are important in Cr(VI)-induced inflammation and after transformation a constitutively high level of Nrf2 is important.

Indexed as

Cell LineCell Transformation, NeoplasticChromiumCyclooxygenase 2HumansNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesTumor Necrosis Factor-alphaChromiumchromium hexavalent ionCyclooxygenase 2NFE2L2 protein, humanNF-E2-Related Factor 2PTGS2 protein, humanReactive Oxygen SpeciesTumor Necrosis Factor-alphaHexavalent chromiumInflammationNrf2ROSTransformed cells

Identifiers

PMID27470422
PMCPMC5527995
OpenAlexW2476499886

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Registered trials

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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.