Evidence map›Paper›PMID 26540468›Full record

ArticleOncotarget2015

Screening key microRNAs for castration-resistant prostate cancer based on miRNA/mRNA functional synergistic network.

Jin Zhu, Sugui Wang, Wenyu Zhang, Junyi Qiu, Yuxi Shan, Dongrong Yang, Bairong Shen

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 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Cancer secretome: finding out hidden messages in extracellular secretions.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  7. Role of miRNA-145, 148, and 185 and Stem Cells in Prostate Cancer.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
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  12. 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 2 institutions in 1 country.

Jin ZhuDepartment of Urology, Second Affiliated Hospital of Soochow University, Suzhou, China.
Sugui WangDepartment of Urology, Second Affiliated Hospital of Soochow University, Suzhou, China.
Wenyu ZhangCenter for Systems Biology, Soochow University, Suzhou, China.
Junyi QiuDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Yuxi ShanDepartment of Urology, Second Affiliated Hospital of Soochow University, Suzhou, China.
Dongrong YangDepartment of Urology, Second Affiliated Hospital of Soochow University, Suzhou, China.
Bairong ShenCenter for Systems Biology, Soochow University, Suzhou, China.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-throughput methods have been used to explore the mechanisms by which androgen-sensitive prostate cancer (ASPC) develops into castration-resistant prostate cancer (CRPC). However, it is difficult to interpret cryptic results by routine experimental methods. In this study, we performed systematic and integrative analysis to detect key miRNAs that contribute to CRPC development. From three DNA microarray datasets, we retrieved 11 outlier microRNAs (miRNAs) that had expression discrepancies between ASPC and CRPC using a specific algorithm. Two of the miRNAs (miR-125b and miR-124) have previously been shown to be related to CRPC. Seven out of the other nine miRNAs were confirmed by quantitative PCR (Q-PCR) analysis. MiR-210, miR-218, miR-346, miR-197, and miR-149 were found to be over-expressed, while miR-122, miR-145, and let-7b were under-expressed in CRPC cell lines. GO and KEGG pathway analyses revealed that miR-218, miR-197, miR-145, miR-122, and let-7b, along with their target genes, were found to be involved in the PI3K and AKT3 signaling network, which is known to contribute to CRPC development. We then chose five miRNAs to verify the accuracy of the analysis. The target genes of each miRNA were altered significantly upon transfection of specific miRNA mimics in the C4-2 CRPC cell line, which was consistent with our pathway analysis results. Finally, we hypothesized that miR-218, miR-145, miR-197, miR-149, miR-122, and let-7b may contribute to the development of CRPC through the influence of Ras, Rho proteins, and the SCF complex. Further investigation is needed to verify the functions of the identified novel pathways in CRPC development.

Indexed as

Blotting, WesternCell Line, TumorGene Expression ProfilingGene Regulatory NetworksHumansMaleMicroRNAsOligonucleotide Array Sequence AnalysisProstatic Neoplasms, Castration-ResistantReal-Time Polymerase Chain ReactionRNA, MessengerTransfectionMicroRNAsRNA, Messengerbioinformatics modelcastration-resistant prostate cancermicroRNA biomarkermicroRNA-mRNA interactionpathway analysis

Identifiers

PMID26540468
PMCPMC4791269
OpenAlexW2096435311

What Socratic 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 Socratic graph.