Evidence map›Paper›PMID 26918939›Full record

ArticleOncotarget2016

MicroRNA-199a and -214 as potential therapeutic targets in pancreatic stellate cells in pancreatic tumor.

Praneeth R Kuninty, Linda Bojmar, Vegard Tjomsland, Marie Larsson, Gert Storm, Arne Östman, Per Sandström, Jai Prakash

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.6field-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

51 citing papers in PubMed, 89 citations in OpenAlex.

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  10. Stroma-derived miR-214 coordinates tumor dissemination.Journal of experimental & clinical cancer research : CR · 2023
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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 6 institutions in 4 countries.

Praneeth R KunintyDepartment of Biomaterials, Science and Technology, Section: Targeted Therapeutics, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Twente, Netherlands.
Linda BojmarDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Vegard TjomslandDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Marie LarssonDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Gert StormDepartment of Biomaterials, Science and Technology, Section: Targeted Therapeutics, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Twente, Netherlands.
Arne ÖstmanDepartment of Oncology-Pathology, Cancer Centre Karolinska, Karolinska Institutet, Karolinska, Sweden.
Per SandströmDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Jai PrakashDepartment of Biomaterials, Science and Technology, Section: Targeted Therapeutics, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Twente, Netherlands.
Karolinska Institutet · SELinköping University · SECornell University · USUniversity of Oslo · NOUniversity of Twente · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic stellate cells (PSCs) are the key precursor cells for cancer-associated fibroblasts (CAFs) in pancreatic tumor stroma. In this study, we explored miRNA as therapeutic targets in tumor stroma and found miR-199a-3p and miR-214-3p induced in patient-derived pancreatic CAFs and TGF-β-activated human PSCs (hPSCs). Inhibition of miR-199a/-214 using hairpin inhibitors significantly inhibited TGFβ-induced differentiation markers (e.g. α-SMA, collagen, PDGFβR), migration and proliferation. Furthermore, heterospheroids of Panc-1 and hPSCs attained smaller size with hPSCs transfected with anti-miR-199a/-214 compared to control anti-miR. The conditioned medium obtained from TGFβ-activated hPSCs induced tumor cell growth and endothelial cell tube formation. Interestingly, these inductions were abrogated in hPSCs transfected with anti-miR-199a or miR-214. Moreover, IPA analyses revealed signaling pathways related to miR-199a (TP53, mTOR, Smad1) and miR-214 (PTEN, Bax, ING4). Taken together, this study reveals miR-199a-3p and miR-214-3p as major regulators of PSC activation and PSC-induced pro-tumoral effects, representing them as key therapeutic targets in pancreatic cancer.

Indexed as

AntagomirsApoptosisCancer-Associated FibroblastsCell DifferentiationCell Line, TumorCell MovementCell ProliferationCells, CulturedGene Expression Regulation, NeoplasticHumansIn Situ HybridizationMicroRNAsPancreatic NeoplasmsPancreatic Stellate CellsReverse Transcriptase Polymerase Chain ReactionSignal TransductionAntagomirsMicroRNAsmirn199 microRNA, humanMIRN214 microRNA, humanTransforming Growth Factor beta1cancer-associated fibroblastsmiRNApancreatic cancerpancreatic stellate cellsstroma

Identifiers

PMID26918939
PMCPMC4941323
OpenAlexW2268705481

What OpenQuestion holds

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LicenceCC BY
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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.