Evidence map›Paper›PMID 34209278›Full record

ArticleCells2021

NOX4 Signaling Mediates Cancer Development and Therapeutic Resistance through HER3 in Ovarian Cancer Cells.

Wen-Jing Liu, Ying-Xue Huang, Wei Wang, Ye Zhang, Bing-Jie Liu, Jian-Ge Qiu, Bing-Hua Jiang, Ling-Zhi Liu

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.3field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. A narrative review ofFrontiers in oncology · 2026
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  7. Article
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  9. Article
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  11. Article
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  14. Article
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  16. Article
  17. NADPH Oxidase 4: A Potential Therapeutic Target of Malignancy.Frontiers in cell and developmental biology · 2022
    Review
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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 2 institutions in 2 countries.

Wen-Jing LiuSchool of Basic Medical Science, Academy of Medical Science, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450001, China.ORCID 0000-0003-1242-5228
Ying-Xue HuangSchool of Basic Medical Science, Academy of Medical Science, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450001, China.
Wei WangSchool of Basic Medical Science, Academy of Medical Science, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450001, China.
Ye ZhangSchool of Basic Medical Science, Academy of Medical Science, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450001, China.
Bing-Jie LiuSchool of Basic Medical Science, Academy of Medical Science, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450001, China.
Jian-Ge QiuSchool of Basic Medical Science, Academy of Medical Science, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou 450001, China.
Bing-Hua JiangDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.ORCID 0000-0003-4526-2031
Ling-Zhi LiuDepartment of Medical Oncology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Zhengzhou University · CNThomas Jefferson University · US

Funding

National Natural Science Foundation of China no. 81903174Postdoctoral Research Grant in Henan Province no. 001803002the Science and Technology Research Project of Henan province no. 202102310418
6 · The paper itself

Abstract

Development of resistance to therapy in ovarian cancer is a major hinderance for therapeutic efficacy; however, new mechanisms of the resistance remain to be elucidated. NADPH oxidase 4 (NOX4) is responsible for higher NADPH activity to increase reactive oxygen species (ROS) production. In this study, we showed that higher levels of NOX4 were detected in a large portion of human ovarian cancer samples. To understand the molecular mechanism of the NOX4 upregulation, we showed that NOX4 expression was induced by HIF-1α and growth factor such as IGF-1. Furthermore, our results indicated that NOX4 played a pivotal role in chemotherapy and radiotherapy resistance in ovarian cancer cells. We also demonstrated that NOX4 knockdown increased sensitivity of targeted therapy and radiotherapy through decreased expression of HER3 (ERBB3) and NF-κB p65. Taken together, we identified a new HIF-1α/NOX4 signal pathway which induced drug and radiation resistance in ovarian cancer. The finding may provide a new option to overcome the therapeutic resistance of ovarian cancer in the future.

Indexed as

Drug Resistance, NeoplasmSignal TransductionAfatinibAlternative SplicingCarcinogenesisCell Line, TumorDown-RegulationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHypoxia-Inducible Factor 1, alpha SubunitInsulin-Like Growth Factor IModels, BiologicalNADPH Oxidase 4Ovarian NeoplasmsAfatinibERBB3 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitInsulin-Like Growth Factor INADPH Oxidase 4Receptor, ErbB-3Transcription Factor RelATrastuzumabHER3HIF-1αNOX4ovarian cancertherapeutic resistance

Identifiers

PMID34209278
PMCPMC8304464
OpenAlexW3176266932

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.