Evidence map›Paper›PMID 23661430›Full record

ArticleMolecular carcinogenesis2014

Putative tumor suppressor gene SEL1L was downregulated by aberrantly upregulated hsa-mir-155 in human pancreatic ductal adenocarcinoma.

Qian Liu, Jinyun Chen, Jin Wang, Christopher Amos, Ann M Killary, Subrata Sen, Chongjuan Wei, Marsha L Frazier

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025
    Review
  3. Review
  4. Pancreatic Cancer: Genetic Conditions and Epigenetic Alterations.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Possible Molecular Markers for the Diagnosis of Pancreatic Ductal Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  14. MicroRNAs in pancreatic cancer diagnosis and therapy.Central-European journal of immunology · 2018
    Review
  15. Article
  16. MicroRNA in pancreatic cancer.Journal of human genetics · 2017
    Review
  17. Article
  18. Pancreatic Cancer, A Mis-interpreter of the Epigenetic Language.The Yale journal of biology and medicine · 2016
    Review
  19. Article
  20. MicroRNA-155 promotes apoptosis in SKOV3, A2780, and primary cultured ovarian cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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 1 institution in 1 country.

Qian LiuDepartment of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jinyun Chen
Jin Wang
Christopher Amos
Ann M Killary
Subrata Sen
Chongjuan Wei
Marsha L Frazier
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
Center for Clinical and Translational Sciences (CCTS)UL1TR000371 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2012 to 2016
$13.4M
CANCER PREVENTION EDUCAT--STUDENT RESEARCH EXPERIENCESR25CA056452 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Shine Chang · 1992 to 2026
$6.9M
Biomarkers for the Early Detection of Pancreatic CancerU01CA111302 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KILLARY, ANN M, SEN, SUBRATA · 2004 to 2015
$6.6M
SPORE in Pancreatic CancerP20CA101936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ABBRUZZESE, JAMES L. · 2003 to 2009
$5.4M
MOLECULAR GENETICS OF HNPCCR01CA070759 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FRAZIER, MARSHA L. · 1997 to 2011
$4.4M
Mouse Model of Pancreatic Tumorigenesis with Dysregulation of mTORR03CA132103 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WEI, CHONGJUAN · 2008 to 2009
$154k
MOUSE MODEL FOR THE PEUTZ JEGHERS SYNDROMER03CA089843 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI FRAZIER, MARSHA L. · 2001 to 2002
$150k
Intramural NIH HHS Z99 CA999999NCATS NIH HHS UL1 TR000371NCI NIH HHS CA016672NCI NIH HHS P20 CA101936NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA023108NCI NIH HHS R01 CA070759NCI NIH HHS R03 CA089843NCI NIH HHS R03 CA132103NCI NIH HHS R25 CA056452NCI NIH HHS R25 CA56452NCI NIH HHS U01 CA111302
6 · The paper itself

Abstract

Sel-1-like (SEL1L) is a putative tumor suppressor gene that is significantly downregulated in human pancreatic ductal adenocarcinoma (PDA). The mechanism of the downregulation is unclear. Here, we investigated whether aberrantly upregulated microRNAs (miRNAs) repressed the expression of SEL1L. From reported miRNA microarray studies on PDA and predicted miRNA targets, we identified seven aberrantly upregulated miRNAs that potentially target SEL1L. We assessed the expression levels of SEL1L mRNA and the seven miRNAs in human PDA tumors and normal adjacent tissues using real-time quantitative polymerase chain reaction. Then statistical methods were applied to evaluate the association between SEL1L mRNA and the miRNAs. Furthermore, the interaction was explored by functional analysis, including luciferase assay and transient miRNA overexpression. SEL1L mRNA expression levels were found to correlate inversely with the expression of hsa-mir-143, hsa-mir-155, and hsa-mir-223 (P < 0.0001, P < 0.0001, and P = 0.002, respectively). As the number of these overexpressed miRNAs increased, SEL1L mRNA expression progressively decreased (Ptrend  = 0.001). Functional analysis revealed that hsa-mir-155 acted as a suppressor of SEL1L in PDA cell lines. Our study combined statistical analysis with biological approaches to determine the relationships between several miRNAs and the SEL1L gene. The finding that the expression of the putative tumor suppressor SEL1L is repressed by upregulation of hsa-mir-155 helps to elucidate the mechanism for SEL1L downregulation in some human PDA cases. Our results suggest a role for specific miRNAs in the pathogenesis of PDA and indicate that miRNAs have potential as therapeutic targets for PDA.

Indexed as

Gene Expression Regulation, NeoplasticBiomarkers, TumorBlotting, WesternCarcinoma, Pancreatic DuctalCells, CulturedGene Expression ProfilingHumansLuciferasesMicroRNAsOligonucleotide Array Sequence AnalysisPancreasPancreatic NeoplasmsProtein Array AnalysisProteinsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionBiomarkers, TumorLuciferasesMicroRNAsMIRN155 microRNA, humanProteinsRNA, MessengerSEL1L protein, humangene expression regulationIngenuity Pathways AnalysismicroRNAreverse phase protein assay

Identifiers

PMID23661430
PMCPMC3887131
OpenAlexW2163859244

What OpenQuestion holds

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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.