Evidence map›Paper›PMID 25310533›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2014

Downregulation of spleen tyrosine kinase in hepatocellular carcinoma by promoter CpG island hypermethylation and its potential role in carcinogenesis.

So-Hyun Shin, Kwang Ho Lee, Baek-Hee Kim, Sun Lee, Hwan Seok Lee, Ja-June Jang, Gyeong Hoon Kang

Abstract read
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In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Role of spleen tyrosine kinase in liver diseases.World journal of gastroenterology · 2020
    Review
  6. Article
  7. Article
  8. 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

7 authors at 4 institutions in 2 countries.

So-Hyun ShinLaboratory of Epigenetics, Cancer Research Institute, Brain Korea 21 PLUS, Seoul National University, Seoul, Korea.
Kwang Ho LeeDepartments of Surgery and of Biochemistry and Molecular Biology, USC Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Baek-Hee KimDepartment of Pathology, Korea University, Seoul, Korea.
Sun LeeDepartment of Pathology, Kyung Hee University, Seoul, Korea.
Hwan Seok LeeDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Ja-June JangDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Gyeong Hoon Kang1] Laboratory of Epigenetics, Cancer Research Institute, Brain Korea 21 PLUS, Seoul National University, Seoul, Korea [2] Department of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Seoul National University · KRKorea University · KRKyung Hee University · KRUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spleen tyrosine kinase (SYK) has predominantly been studied in hematopoietic cells, where it is involved in immunoreceptor-mediated signaling. However, SYK expression has been shown in numerous non-hematopoietic cells, and its downregulation has been shown to be involved in tumor formation and progression. SYK methylation has been demonstrated to identify a subset of hepatocellular carcinoma (HCC) cases with poor prognosis, but little is known regarding the biological role of SYK in HCC. We found that SYK methylation is a common event in HCC, and is inversely associated with its expression. We established stable HCC cell lines with inducible SYK expression vectors, and compared the differential RNA expression profiles of HCC cell lines with or without the induction of SYK. Gene ontology analysis revealed that the SYK-regulated genes were enriched for genes involved in cell adhesion. Accordingly, we found that the induction of SYK expression increased the adhesion of cells to fibronectin and decreased cell migration and invasion, and that cessation of SYK overexpression increased cell migration and invasion. Our findings suggest that SYK is involved in regulating cell to matrix adhesions, and that SYK loss affects the migration, and invasion of HCC cells.

Indexed as

CpG IslandsDNA MethylationPromoter Regions, GeneticAdultAgedCarcinogenesisCarcinoma, HepatocellularCell Line, TumorCell ProliferationDown-RegulationFemaleGene Expression ProfilingHumansIntegrin beta1Intracellular Signaling Peptides and ProteinsLiver NeoplasmsIntegrin beta1Intracellular Signaling Peptides and ProteinsProtein-Tyrosine KinasesSyk KinaseSYK protein, human

Identifiers

PMID25310533
OpenAlexW2023452119

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.