Evidence map›Paper›PMID 27825122›Full record

ArticleOncotarget2016

Identification and validation of differentially expressed proteins in epithelial ovarian cancers using quantitative proteomics.

Hong Qu, Yuling Chen, Guangming Cao, Chongdong Liu, Jiatong Xu, Haiteng Deng, Zhenyu Zhang

Open access · diamondAbstract readValidation Study
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  5. Ion Channels and Personalized Medicine in Gynecological Cancers.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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  8. Review
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  11. Article
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  16. Dlg1 Maintains Dendritic Cell Function by Securing Voltage-Gated KJournal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  17. Review
  18. Article
  19. 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

7 authors at 4 institutions in 1 country.

Hong QuDepartment of Obstetrics & Gynecology, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing, China.
Yuling ChenTsinghua University-Peking University Joint Center for Life Sciences, Beijing, China.
Guangming CaoDepartment of Obstetrics & Gynecology, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing, China.
Chongdong LiuDepartment of Obstetrics & Gynecology, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing, China.
Jiatong XuMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing, China.
Haiteng DengMOE Key Laboratory of Bioinformatics, School of Life Sciences, Tsinghua University, Beijing, China.
Zhenyu ZhangDepartment of Obstetrics & Gynecology, Beijing Chao-yang Hospital Affiliated to Capital Medical University, Beijing, China.
Beijing Chao-Yang Hospital · CNCapital Medical University · CNTsinghua University · CNCenter for Life Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecological malignant tumor because of its high recurrence rate. In the present work, in order to find new therapeutic targets, we identified 8480 proteins in thirteen pairs of ovarian cancer tissues and normal ovary tissues through quantitative proteomics. 498 proteins were found to be differentially expressed in ovarian cancer, which involved in various cellular processes, including metabolism, response to stimulus and biosynthetic process. The expression levels of chloride intracellular channel protein 1 (CLIC1) and lectin galactoside-binding soluble 3 binding protein (LGALS3BP) in epithelial ovarian cancer tissues were significantly higher than those in normal ovary tissues as confirmed by western blotting and immunohistochemistry. The knockdown of CLIC1 in A2780 cell line downregulated expression of CTPS1, leading to the decrease of CTP and an arrest of cell cycle G1 phase, which results into a slower proliferation. CLIC1-knockdown can also slow down the tumor growth in vivo. Besides, CLIC1-knockdown cells showed an increased sensitivity to hydrogen peroxide and cisplatin, suggesting that CLIC1 was involved in regulation of redox and drug resistance in ovarian cancer cells. These results indicate CLIC1 promotes tumorgenesis, and is a potential therapeutic target in epithelial ovarian cancer treatment.

Indexed as

AnimalsAntigens, NeoplasmAntineoplastic AgentsBiomarkers, TumorCarbon-Nitrogen LigasesCarcinoma, Ovarian EpithelialCarrier ProteinsCell Line, TumorCell ProliferationChloride ChannelsCisplatinCytidine TriphosphateDose-Response Relationship, DrugDrug Resistance, NeoplasmExtracellular Matrix ProteinsFemaleAntigens, NeoplasmAntineoplastic AgentsBiomarkers, TumorCarbon-Nitrogen LigasesCarrier ProteinsChloride ChannelsCisplatinCLIC1 protein, humanCTP synthetaseCytidine TriphosphateExtracellular Matrix ProteinsGlycoproteinsHydrogen PeroxideLGALS3BP protein, humanCLIC1epithelial ovarian cancerLGALS3BPproteomicstherapeutic target

Identifiers

PMID27825122
PMCPMC5347761
OpenAlexW2548311895

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.