Evidence map›Paper›PMID 33107155›Full record

ArticleJournal of cellular and molecular medicine2020

Comprehensive role of prostate-specific antigen identified with proteomic analysis in prostate cancer.

Haoyong Li, Zhe Ma, Zhifei Che, Qi Li, Jinfeng Fan, Zhiyan Zhou, Yaoxi Wu, Yingxia Jin, Peiyu Liang, Xianping Che

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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 2 institutions in 1 country.

Haoyong LiDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, China.
Zhe MaDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Zhifei CheDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Qi LiDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Jinfeng FanDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Zhiyan ZhouDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Yaoxi WuDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Yingxia JinCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Peiyu LiangDepartment of Urology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.ORCID 0000-0002-2048-0502
Xianping CheDepartment of Urology, The Second Affiliated Hospital of Hainan Medical University, Haikou, China.
Hainan Medical University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current treatments including androgen deprivation fail to prevent prostate cancer (PrCa) from progressing to castration-resistant PrCa (CRPC). Accumulating evidence highlights the relevance of prostate-specific antigen (PSA) in the development and progression of PrCa. The underlying mechanism whereby PSA functions in PrCa, however, has yet been elucidated. We demonstrated that PSA knockdown attenuated tumorigenesis and metastasis of PrCa C4-2 cells in vitro and in vivo, whereas promoted the apoptosis in vitro. To illuminate the comprehensive role of PSA in PrCa, we performed an isobaric tag for relative and absolute quantitation (iTRAQ)-based proteomic analysis to explore the proteomic change induced by PSA knockdown. Among 121 differentially expressed proteins, 67 proteins were up-regulated, while 54 proteins down-regulated. Bioinformatics analysis was used to explore the mechanism through which PSA exerts influence on PrCa. Protein-protein interaction analysis showed that PSA may mediate POTEF, EPHA3, RAD51C, HPGD and MCM4 to promote the initiation and progression of PrCa. We confirmed that PSA knockdown induced the up-regulation of MCM4 and RAD51C, while it down-regulated POTEF and EPHA3; meanwhile, MCM4 was higher in PrCa para-cancerous tissue than in cancerous tissue, suggesting that PSA may facilitate the tumorigenesis by mediating MCM4. Our findings suggest that PSA plays a comprehensive role in the development and progression of PrCa.

Indexed as

Cell Line, TumorDisease ProgressionHumansMaleProstate-Specific AntigenProstatic NeoplasmsProtein Interaction MapsProteomeProteomicsUp-RegulationProstate-Specific AntigenProteomeiTRAQMCM4prostate cancerprostate‐specific antigenproteomic analysis

Identifiers

PMID33107155
PMCPMC7520270
OpenAlexW3045818159

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.