Evidence map›Paper›PMID 28397780›Full record

ArticleNature communications2017

Computational identification of mutually exclusive transcriptional drivers dysregulating metastatic microRNAs in prostate cancer.

Mengzhu Xue, Haiyue Liu, Liwen Zhang, Hongyuan Chang, Yuwei Liu, Shaowei Du, Yingqun Yang, Peng Wang

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 20 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

8 authors at 2 institutions in 1 country.

Mengzhu XueLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.
Haiyue LiuLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.
Liwen ZhangShanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Zhang Jiang Hi-Tech Park, Pudong, Shanghai 201203, China.
Hongyuan ChangLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.
Yuwei LiuLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.
Shaowei DuLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.
Yingqun YangLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.
Peng WangLaboratory of Systems Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 100 Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China.ORCID 0000-0002-2972-7495
Chinese Academy of Sciences · CNShanghai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen-ablation therapies, which are the standard treatment for metastatic prostate cancer, invariably lead to acquired resistance. Hence, a systematic identification of additional drivers may provide useful insights into the development of effective therapies. Numerous microRNAs that are critical for metastasis are dysregulated in metastatic prostate cancer, but the underlying molecular mechanism is poorly understood. We perform an integrative analysis of transcription factor (TF) and microRNA expression profiles and computationally identify three master TFs, AR, HOXC6 and NKX2-2, which induce the aberrant metastatic microRNA expression in a mutually exclusive fashion. Experimental validations confirm that the three TFs co-dysregulate a large number of metastasis-associated microRNAs. Moreover, their overexpression substantially enhances cell motility and is consistently associated with a poor clinical outcome. Finally, the mutually exclusive overexpression between AR, HOXC6 and NKX2-2 is preserved across various tissues and cancers, suggesting that mutual exclusivity may represent an intrinsic characteristic of driver TFs during tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticCell LineCell Line, TumorComputational BiologyGene Expression ProfilingHomeobox Protein Nkx-2.2Homeodomain ProteinsHumansMaleMicroRNAsNeoplasm MetastasisNuclear ProteinsProstatic NeoplasmsReceptors, AndrogenTranscription FactorsZebrafish ProteinsHomeobox Protein Nkx-2.2Homeodomain ProteinsHOXC6 protein, humanMicroRNAsnkx2.2b protein, zebrafishNKX2-2 protein, humanNuclear ProteinsReceptors, AndrogenTranscription FactorsZebrafish Proteins

Identifiers

PMID28397780
PMCPMC5394245
OpenAlexW2605758741

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.