Evidence map›Paper›PMID 32414223›Full record

ArticleCancers2020

LINC00261 Is Differentially Expressed in Pancreatic Cancer Subtypes and Regulates a Pro-Epithelial Cell Identity.

Agnes Dorn, Markus Glaß, Carolin T Neu, Beate Heydel, Stefan Hüttelmaier, Tony Gutschner, Monika Haemmerle

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  5. Clinical Significance ofDiseases (Basel, Switzerland) · 2025
    Review
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  7. Article
  8. Review
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  10. The inhibitory effect of LINC00261 upregulation on the pancreatic cancer EMT process is mediated by KLF13 via the mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  11. Review
  12. Article
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  16. Article
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  19. Post-Transcriptional Expression Control in Platelet Biogenesis and Function.International journal of molecular sciences · 2020
    Review
  20. Review
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

7 authors at 1 institution in 1 country.

Agnes DornInstitute of Pathology, Section for Experimental Pathology, Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Markus GlaßInstitute of Molecular Medicine, Section for Cell Biology, Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Carolin T NeuInstitute of Pathology, Section for Experimental Pathology, Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Beate HeydelInstitute of Pathology, Section for Experimental Pathology, Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Stefan HüttelmaierInstitute of Molecular Medicine, Section for Cell Biology, Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Tony GutschnerJunior Research Group 'RNA biology and Pathogenesis', Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Monika HaemmerleInstitute of Pathology, Section for Experimental Pathology, Medical Faculty, Martin-Luther University Halle-Wittenberg, 06120 Halle/Saale, Germany.
Martin Luther University Halle-Wittenberg · DE

Funding

Wilhelm Roux Program, Medical Faculty, Martin Luther University Halle-Wittenberg FKZ 31/18
6 · The paper itself

Abstract

Pancreatic adenocarcinoma (PDAC) is one of the major causes of cancer-associated deaths worldwide, with a dismal prognosis that has not significantly changed over the last decades. Transcriptional analysis has provided valuable insights into pancreatic tumorigenesis. Specifically, pancreatic cancer subtypes were identified, characterized by specific mutations and gene expression changes associated with differences in patient survival. In addition to differentially regulated mRNAs, non-coding RNAs, including long non-coding RNAs (lncRNAs), were shown to have subtype-specific expression patterns. Hence, we aimed to characterize prognostic lncRNAs with deregulated expression in the squamous subtype of PDAC, which has the worst prognosis. Extensive in silico analyses followed by in vitro experiments identified long intergenic non-coding RNA 261 (LINC00261) as a downregulated lncRNA in the squamous subtype of PDAC, which is generally associated with transforming growth factor β (TGFβ) signaling in human cancer cells. Its genomic neighbor, the transcription factor forkhead box protein A2 (FOXA2), regulated LINC00261 expression by direct binding of the LINC00261 promoter. CRISPR-mediated knockdown and promoter knockout validated the importance of LINC00261 in TGFβ-mediated epithelial-mesenchymal transition (EMT) and established the epithelial marker E-cadherin, an important cell adhesion protein, as a downstream target of LINC00261. Consequently, depletion of LINC00261 enhanced motility and invasiveness of PANC-1 cells in vitro. Altogether, our data suggest that LINC00261 is an important tumor-suppressive lncRNA in PDAC that is involved in maintaining a pro-epithelial state associated with favorable disease outcome.

Indexed as

CDH1EMTFOXA2LINC00261lncRNAPDACTGFβ

Identifiers

PMID32414223
PMCPMC7281485
OpenAlexW3024058030

What OpenQuestion 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 OpenQuestion graph.