Evidence map›Paper›PMID 30580676›Full record

ArticleCancer biology & therapy2019

Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway.

Yuan-Chi Weng, Jin Ma, Jun Zhang, Jian-Cheng Wang

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Review
  9. Article
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  12. A review on the role of LINC01133 in cancers.Cancer cell international · 2022
    Review
  13. Article
  14. Article
  15. Drug Discovery of DKK1 Inhibitors.Frontiers in pharmacology · 2022
    Review
  16. Review
  17. Review
  18. Article
  19. Regulation of Hippo, TGFβ/SMAD, Wnt/Frontiers in oncology · 2021
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yuan-Chi Wenga Department of General Surgery , Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine , Shanghai , P.R. China.
Jin Mab Department of Gastroenterology , Luwan Branch of Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine , Shanghai , P.R. China.
Jun Zhanga Department of General Surgery , Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine , Shanghai , P.R. China.
Jian-Cheng Wanga Department of General Surgery , Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine , Shanghai , P.R. China.
Ruijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have acknowledged the critical roles played by long non-coding RNAs (lncRNAs) in the development and progression of pancreatic cancer. Therefore, the present study aimed to elucidate the mechanism underlying on how LINC01133 regulates the Wnt signaling pathway in pancreatic cancer. A microarray-based gene expression analysis was performed to identify the differentially expressed lncRNAs in pancreatic cancer. In addition, ectopic expression assays, knockdown experiments and gene reporter assays were conducted to clarify the role of LINC01133 in pancreatic cancer and to understand the interaction between LINC01133 and the methylation of DKK1 promoter. The expression of LINC01133, DKK1, and other genes related to the Wnt signaling pathway was also measured. EDU staining, scratch test and Transwell assay were employed to measure the proliferation, migration and invasion of pancreatic cancer cells, respectively. GSE32676 and GSE16515 revealed that LINC01133 was upregulated in pancreatic cancer, which was also associated with increased DKK1 methylation and higher expression of genes related to the Wnt signaling pathway, although the expression of DKK1 decreased in pancreatic cancer. In addition, LINC01133 bound to the promoter region of DKK1, resulting in the trimethylation of H3K27 and decreased DKK1 expression, while the expression of Wnt-5a, MMP-7, and β-catenin increased upon LINC01133 binding. Finally, over-expressed LINC01133 enhanced the growth, proliferation, migration, metastasis, and invasion of pancreatic cancer cells. The present study clarified the distinct effect of LINC01133 on pancreatic cancer. In summary, by inducing the methylation of DKK1 promoter, LINC01133 silencing suppresses the development of pancreatic cancer cells through the Wnt signaling pathway.

Indexed as

DNA MethylationWnt Signaling PathwayAnimalsCell Line, TumorCell MovementCell ProliferationDisease ProgressionHeterograftsHumansIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessOligonucleotide Array Sequence AnalysisDKK1 protein, humanIntercellular Signaling Peptides and Proteinslong non-coding RNA LINC01133, humanRNA, Long NoncodingDKK1invasionLINC01133methylationmigrationpancreatic cancerproliferation

Identifiers

PMID30580676
PMCPMC6370374
OpenAlexW2905797460

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.