Evidence map›Paper›PMID 23264205›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2013

CD81 is a candidate tumor suppressor gene in human gastric cancer.

Tae-Hyoung Yoo, Byung-Kyu Ryu, Min-Goo Lee, Sung-Gil Chi

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  14. Increased expression ofExperimental and therapeutic medicine · 2020
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  16. Prostate cancer sheds the αvβ3 integrin in vivo through exosomes.Matrix biology : journal of the International Society for Matrix Biology · 2019
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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

4 authors at 1 institution in 1 country.

Tae-Hyoung YooSchool of Life Sciences and Biotechnology, Korea University, 136-701, Seoul, Republic of Korea.
Byung-Kyu Ryu
Min-Goo Lee
Sung-Gil Chi
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD81 is a transmembrane protein that serves as a putative receptor for hepatitis C virus. In addition, CD81 has been suggested to be involved in a broad range of other cellular functions. Its putative implication in tumorigenesis has so far, however, remained largely unexplored. To assess the candidacy of CD81 as a tumor suppressor in gastric cancer development, we investigated its expression and function in a series of primary gastric tumors and gastric tumor-derived cell lines.

methodsThe expression and concomitant methylation status of the CD81 gene and its effect on tumor development and cellular signaling were evaluated.

resultsCD81 mRNA levels were found to be low in 16 of 40 (40 %) primary tumors and 9 of 14 (64.2 %) cell lines, and these low expression levels were found to correlate with the stage and grade of the tumors. Genomic alterations of CD81 were not encountered, whereas its expression could be re-activated in low expressing cells upon 5-aza-dC treatment. Bisulfite DNA sequencing analysis of 10 CpG sites within the 5' proximal region of the CD81 gene promoter revealed that the observed transcriptional silencing was tightly associated with aberrant hypermethylation. Subsequent restoration of CD81 expression induced a G1 cell cycle arrest and apoptosis, whereas siRNA-mediated CD81 down-regulation promoted cell proliferation and attenuated cellular responses to various apoptotic stress stimuli. Also the colony-forming ability of the tumor cells could be inhibited and enhanced through CD81 up- and down-regulation, respectively. CD81 was found to inhibit p38 (but not ERK, JNK and AKT) phosphorylation and its growth suppressive effect could be abolished through p38 up- and down-regulation.

conclusionFrom our data we conclude that epigenetic inactivation of CD81 is a common feature of gastric tumors and that this inactivation may render growth and survival advantages to the tumor cells, at least partially through p38 signaling.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisAzacitidineBase SequenceBlotting, WesternCell CycleCell Line, TumorDecitabineDisease ProgressionDNA MethylationDown-RegulationG1 Phase Cell Cycle CheckpointsHumansMolecular Sequence Datap38 Mitogen-Activated Protein KinasesPhosphorylationAzacitidineCD81 protein, humanDecitabinep38 Mitogen-Activated Protein KinasesTetraspanin 28Tumor Suppressor Proteins

Identifiers

PMID23264205
PMCPMC13012677
OpenAlexW2035480831

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.