Evidence map›Paper›PMID 26095125›Full record

ArticleScientific reports2015

Pathophysiological role of microRNA-29 in pancreatic cancer stroma.

Jason J Kwon, Sarah C Nabinger, Zachary Vega, Smiti Snigdha Sahu, Ravi K Alluri, Zahi Abdul-Sater, Zhangsheng Yu, Jesse Gore, Grzegorz Nalepa, Romil Saxena and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. miRNAs in pancreatic cancer progression and metastasis.Clinical & experimental metastasis · 2024
    Review
  4. Review
  5. Review
  6. The Role of MicroRNAs in Pancreatitis Development and Progression.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. The role of miR-29 family in disease.Journal of cellular biochemistry · 2021
    Review
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

12 authors at 3 institutions in 1 country.

Jason J KwonDepartment of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA.
Sarah C NabingerDepartment of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA.
Zachary VegaWabash College, Crawfordsville, IN, USA.
Smiti Snigdha Sahu1] Department of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA [2] Department of Pathology, IUSM, Indianapolis, IN, USA.
Ravi K AlluriDepartment of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA.
Zahi Abdul-SaterDepartment of Biochemistry and Molecular Biology, IUSM, Indianapolis, IN, USA.
Zhangsheng YuDepartment of Biostatistics, IUSM, Indianapolis, IN, USA.
Jesse Gore1] Department of Medicine, IUSM, Indianapolis, IN, USA [2] The Melvin and Bren Simon Cancer Center, IUSM, Indianapolis, IN, USA [3] Center for Pancreatic Cancer Research, Indiana University and Purdue University-Indianapolis (IUPUI), Indianapolis, IN, USA.
Grzegorz Nalepa1] Department of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA [2] Department of Biochemistry and Molecular Biology, IUSM, Indianapolis, IN, USA [3] Department of Pediatrics, Herman B Wells Center for Pediatric Research, IUSM, Indianapolis, IN, USA [4] Division of Pediatric Hematology-Oncology, Bone Marrow Failure Program, IUSM, Indianapolis, IN, USA.
Romil SaxenaDepartment of Pathology, IUSM, Indianapolis, IN, USA.
Murray Korc1] Department of Biochemistry and Molecular Biology, IUSM, Indianapolis, IN, USA [2] Department of Medicine, IUSM, Indianapolis, IN, USA [3] The Melvin and Bren Simon Cancer Center, IUSM, Indianapolis, IN, USA [4] Center for Pancreatic Cancer Research, Indiana University and Purdue University-Indianapolis (IUPUI), Indianapolis, IN, USA.
Janaiah Kota1] Department of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA [2] The Melvin and Bren Simon Cancer Center, IUSM, Indianapolis, IN, USA [3] Center for Pancreatic Cancer Research, Indiana University and Purdue University-Indianapolis (IUPUI), Indianapolis, IN, USA.
Indiana University – Purdue University Indianapolis · USIndiana University Health · USWabash College · US

Funding

Novel aspects of Epithelial-Mesenchymal Transition(EMT)in pancreatic cancerR01CA075059 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KORC, MURRAY · 1997 to 2018
$4.3M
Dysregulation of TGF Beta Action Pancreatic CancerR37CA075059 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KORC, MURRAY · 2008 to 2012
$2.2M
NCI NIH HHS CA-075059NCI NIH HHS R01 CA075059NCI NIH HHS R37 CA075059
6 · The paper itself

Abstract

Dense fibrotic stroma associated with pancreatic ductal adenocarcinoma (PDAC) is a major obstacle for drug delivery to the tumor bed and plays a crucial role in pancreatic cancer progression. Current, anti-stromal therapies have failed to improve tumor response to chemotherapy and patient survival. Furthermore, recent studies show that stroma impedes tumor progression, and its complete ablation accelerates PDAC progression. In an effort to understand the molecular mechanisms associated with tumor-stromal interactions, using in vitro and in vivo models and PDAC patient biopsies, we show that the loss of miR-29 is a common phenomenon of activated pancreatic stellate cells (PSCs)/fibroblasts, the major stromal cells responsible for fibrotic stromal reaction. Loss of miR-29 is correlated with a significant increase in extracellular matrix (ECM) deposition, a major component in PDAC stroma. Our in vitro miR-29 gain/loss-of-function studies document the role of miR-29 in PSC-mediated ECM stromal protein accumulation. Overexpression of miR-29 in activated stellate cells reduced stromal deposition, cancer cell viability, and cancer growth in co-culture. Furthermore, the loss of miR-29 in TGF-β1 activated PSCs is SMAD3 dependent. These results provide insights into the mechanistic role of miR-29 in PDAC stroma and its potential use as a therapeutic agent to target PDAC.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, Pancreatic DuctalCell Line, TumorCell SurvivalEnzyme ActivationExtracellular MatrixFibroblastsFibrosisHumansMiceMice, Inbred C57BLMice, TransgenicMicroRNAsPancreasPancreatic NeoplasmsAntineoplastic AgentsKRAS protein, humanMicroRNAsMIRN29a microRNA, humanProto-Oncogene Proteins p21(ras)Smad3 ProteinSMAD3 protein, humanTransforming Growth Factor beta

Identifiers

PMID26095125
PMCPMC4476113
OpenAlexW2220916195

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.