Evidence map›Paper›PMID 30033362›Full record

ArticleCell2018

Risk SNP-Mediated Promoter-Enhancer Switching Drives Prostate Cancer through lncRNA PCAT19.

Junjie Tony Hua, Musaddeque Ahmed, Haiyang Guo, Yuzhe Zhang, Sujun Chen, Fraser Soares, Jennifer Lu, Stanley Zhou, Miranda Wang, Hui Li and 13 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed
12.8field-weighted citation impact, top 1% 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

203 citing papers in PubMed, 313 citations in OpenAlex.

  1. Trial
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143 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 5 institutions in 3 countries.

Junjie Tony HuaPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
Musaddeque AhmedPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada.
Haiyang GuoPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada.
Yuzhe ZhangPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; College of Life Sciences, Central China Normal University, Wuhan, Hubei, China; College of Basic Medical Sciences, Dali University, Dali, Yunnan, China.
Sujun ChenPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
Fraser SoaresPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada.
Jennifer LuPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Stanley ZhouPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
Miranda WangPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada.
Hui LiDepartment of Radiation Oncology, University of California at San Francisco, San Francisco, CA, USA.
Nicholas B LarsonDepartment of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
Shannon K McDonnellDepartment of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
Parasvi S PatelPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
Yi LiangPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada.
Cindy Q YaoOntario Institute for Cancer Research, Toronto, ON M5G 0A3, Canada.
Theodorus van der KwastDepartment of Pathology and Laboratory Medicine, Toronto General Hospital/University Health Network, Toronto, ON, Canada.
Mathieu LupienPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada; Ontario Institute for Cancer Research, Toronto, ON M5G 0A3, Canada.
Felix Y FengDepartment of Radiation Oncology, University of California at San Francisco, San Francisco, CA, USA; Department of Urology, University of California at San Francisco, San Francisco, CA, USA; Department of Medicine, University of California at San Francisco, San Francisco, CA, USA; Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA, USA.
Amina ZoubeidiVancouver Prostate Centre, Vancouver, BC V6H 3Z6, Canada.
Ming-Sound TsaoPrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
Stephen N ThibodeauDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
Paul C BoutrosDepartment of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada; Ontario Institute for Cancer Research, Toronto, ON M5G 0A3, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.
Housheng Hansen HePrincess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada. Electronic address: hansenhe@uhnresearch.ca.
University Health Network · CAOntario Institute for Cancer Research · CAMayo Clinic in Florida · USUniversity of California, San Francisco · USMayo Clinic in Arizona · US

Funding

CIHR 142246
6 · The paper itself

Abstract

The prostate cancer (PCa) risk-associated SNP rs11672691 is positively associated with aggressive disease at diagnosis. We showed that rs11672691 maps to the promoter of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long). The risk variant is associated with decreased and increased levels of PCAT19-short and PCAT19-long, respectively. Mechanistically, the risk SNP region is bifunctional with both promoter and enhancer activity. The risk variants of rs11672691 and its LD SNP rs887391 decrease binding of transcription factors NKX3.1 and YY1 to the promoter of PCAT19-short, resulting in weaker promoter but stronger enhancer activity that subsequently activates PCAT19-long. PCAT19-long interacts with HNRNPAB to activate a subset of cell-cycle genes associated with PCa progression, thereby promoting PCa tumor growth and metastasis. Taken together, these findings reveal a risk SNP-mediated promoter-enhancer switching mechanism underlying both initiation and progression of aggressive PCa.

Indexed as

AllelesCell Line, TumorEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGene FrequencyGenetic Predisposition to DiseaseHomeodomain ProteinsHumansMalePolymorphism, Single NucleotidePromoter Regions, GeneticProstatic NeoplasmsProtein BindingRisk FactorsRNA IsoformsRNA, Long NoncodingHomeodomain ProteinsNKX3-1 protein, humanRNA IsoformsRNA, Long NoncodingTranscription FactorsYY1 protein, humanYY1 Transcription Factorbifunctional regulatory elementHNRNPABlncRNANKX3.1PCAT19promoter-enhancer switchingprostate cancer progressionrisk SNPrs11672691YY1

Identifiers

PMID30033362
OpenAlexW2884681204

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.