Evidence map›Paper›PMID 25686830›Full record

ArticleOncotarget2015

p22phox confers resistance to cisplatin, by blocking its entry into the nucleus.

Chih-Chang Hung, Chen-Yu Chien, Wei-Fan Chiang, Chang-Shen Lin, Tzyh-Chyuan Hour, Hau-Ren Chen, Ling-Feng Wang, Jenq-Yuh Ko, Chi-Hua Chang, Jeff Yi-Fu Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Inhibition of p22Journal of Cancer · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. The correlation of p22Oncotarget · 2019
    Article
  11. Article
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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 7 institutions in 1 country.

Chih-Chang HungGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Chen-Yu ChienDepartment of Otorhinolaryngology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Wei-Fan ChiangDepartment of Dentistry, Chi-Mei Medical Center, Liouying, Taiwan.
Chang-Shen LinGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Tzyh-Chyuan HourDepartment of Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan.
Hau-Ren ChenDepartment of Life Science and Institute of Molecular Biology, National Chung Cheng University, Chia-Yi, Taiwan.
Ling-Feng WangDepartment of Otorhinolaryngology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Jenq-Yuh KoDepartment of Otolaryngology, National Taiwan University, College of Medicine, Taipei, Taiwan.
Chi-Hua ChangDepartment of Dentistry, Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Jeff Yi-Fu ChenDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan.
Kaohsiung Medical University · TWKaohsiung Chang Gung Memorial Hospital · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWKaohsiung Municipal Ta-Tung Hospital · TWNational Chung Cheng University · TWNational Taipei University · TWNational Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin (CDDP) is a potent chemotherapeutic agent but resistance to the drug remains a major challenge in cancer treatment. To evaluate the efficacy of CDDP in oral squamous cell carcinoma (OSCC), we found that p22phox was highly expressed in CDDP-resistant OSCC specimens. Knockdown of p22phox sensitized OSCC cell lines to CDDP (P < 0.05). Stable overexpression of p22phox augmented CDDP resistance, as evidenced by the significantly higher IC50 values. This cytoprotective effect was attributed to the abrogation of CDDP-induced apoptosis. Akt phosphorylation was increased in p22phox stable lines. However, blocking PI3K/Akt pathway only partially restored CDDP-induced apoptosis. In addition, the overexpressed p22phox in OSCC cells exhibited cytoplasmic localization with enhanced perinuclear expression, consistent with the localization pattern in OSCC specimens. Remarkably, CDDP entry into the nucleus was severely impaired in p22phox-overexpressing cells (P < 0.001), and cytoplasmically accumulated CDDP was co-localized with overexpressed p22phox. This was supported by decreased CDDP-DNA adduct formation and delayed chk1-p53 signaling activation. Together, overexpression of p22phox sequestered CDDP and caused defective CDDP entry into the nucleus, significantly attenuating CDDP-induced apoptosis. Such diminished apoptosis was further abolished by p22phox-activating PI3K/Akt pathway. Our work has suggested a novel biomarker and insight into the mechanism of CDDP resistance.

Indexed as

Antineoplastic AgentsCarcinoma, Squamous CellCell Line, TumorCell NucleusCisplatinDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesHead and Neck NeoplasmsHumansMaleMiddle AgedMouth NeoplasmsNADPH OxidasesSquamous Cell Carcinoma of Head and NeckUp-RegulationAntineoplastic AgentsCisplatinCYBA protein, humanNADPH Oxidases

Identifiers

PMID25686830
PMCPMC4414176
OpenAlexW1929534795

What OpenQuestion holds

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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.