Evidence map›Paper›PMID 30658679›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

PAGE4 promotes prostate cancer cells survive under oxidative stress through modulating MAPK/JNK/ERK pathway.

Chengcheng Lv, Shui Fu, Qingzhuo Dong, Zi Yu, Gejun Zhang, Chuize Kong, Cheng Fu, Yu Zeng

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  13. Cancer/Testis Antigens as Targets for RNA-Based Anticancer Therapy.International journal of molecular sciences · 2023
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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 1 country.

Chengcheng LvDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, 44 Xiaoheyan Road, Shenyang, 110042, Liaoning, China.
Shui FuDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, 44 Xiaoheyan Road, Shenyang, 110042, Liaoning, China.
Qingzhuo DongDepartment of Urology, The First Hospital of China Medical University, 155 Nanjing North Road, Shenyang, 110001, Liaoning, China.
Zi YuDepartment of Urology, The First Hospital of China Medical University, 155 Nanjing North Road, Shenyang, 110001, Liaoning, China.
Gejun ZhangDepartment of Urology, The First Hospital of China Medical University, 155 Nanjing North Road, Shenyang, 110001, Liaoning, China.
Chuize KongDepartment of Urology, The First Hospital of China Medical University, 155 Nanjing North Road, Shenyang, 110001, Liaoning, China.
Cheng FuDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, 44 Xiaoheyan Road, Shenyang, 110042, Liaoning, China.
Yu ZengDepartment of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, 44 Xiaoheyan Road, Shenyang, 110042, Liaoning, China. zengyud@hotmail.com.
First Hospital of China Medical University · CNLiaoning Cancer Hospital & Institute · CN

Funding

National Natural Science Foundation of China 81372766National Natural Science Foundation of China 81572532
6 · The paper itself

Abstract

backgroundProstate cancer (PCa) is one of the most common cancers in male worldwide. Oxidative stress has been recognized as one of the driving signals pathologically linked to PCa progression. Nevertheless, the association of oxidative stress with PCa progression remains unclear.

methodsWestern blot, q-RT-PCR and bioinformatics analyses were used to examine PAGE4 expression. Comet assay and Annexin V/ PI dual staining assay were performed to investigate DNA damage and cell death under oxidative stress. Mouse xenograft model of PCa cells was established to verify the role of PAGE4 in vivo. Transcriptomic analysis was performed to investigate the underlying mechanism for the function of PAGE4 under oxidative stress. Western blot assay was conducted to determine the status of MAPK pathway. Immunohistochemistry was used to identify protein expression of PAGE4 in tumor tissues.

resultsIn this study, we found that PAGE4 expression was increased in PCa cells under oxidative stress condition. PAGE4 overexpression protected PCa cells from oxidative stress-inducing cell death by reducing DNA damage. PAGE4 overexpression promoted PCa cells growth in vivo. Mechanistically, PAGE4 promoted the survival of prostate cancer cells through regulating MAPK pathway which reflected in decreasing the phosphorylation of MAP2K4, JNK and c-JUN but increasing phosphorylation of ERK1/2.

conclusionOur findings indicate that PAGE4 protects PCa cells from DNA damage and apoptosis under oxidative stress by modulating MAPK signalling pathway. PAGE4 expression may serve as a prognostic biomarker for clinical applications.

Indexed as

MAP Kinase Signaling SystemOxidative StressAnimalsAntigens, NeoplasmCell Line, TumorDisease Models, AnimalGene ExpressionHeterograftsHumansImmunohistochemistryMaleMiceModels, BiologicalPrognosisProstatic NeoplasmsReactive Oxygen SpeciesAntigens, NeoplasmPAGE4 protein, humanReactive Oxygen SpeciesERKMAPKOxidative stressPAGE4Prostate Cancer

Identifiers

PMID30658679
PMCPMC6339303
OpenAlexW2919145100

What OpenQuestion holds

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LicenceCC BY
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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.