Evidence map›Paper›PMID 26472282›Full record

ArticleOncotarget2015

REC8 is a novel tumor suppressor gene epigenetically robustly targeted by the PI3K pathway in thyroid cancer.

Dingxie Liu, Xiaopei Shen, Guangwu Zhu, Mingzhao Xing

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  6. Association of DNA Promoter Methylation andCurrent oncology (Toronto, Ont.) · 2023
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  7. Ectopic expression of meiotic cohesin generates chromosome instability in cancer cell line.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Mesenchymal stem/stromal cells in cancer therapy.Journal of hematology & oncology · 2021
    Review
  12. Article
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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 2 institutions in 1 country.

Dingxie LiuLaboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Xiaopei ShenLaboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Guangwu ZhuLaboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Mingzhao XingLaboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Genetic & Epigenetic Events in Papillary Thyroid CancerR01CA113507 · NCI · JOHNS HOPKINS UNIVERSITY · PI XING, MICHAEL MINGZHAO · 2006 to 2015
$2.2M
Genome-wide Exploration of DNA Methylation Markers for Thyroid CancerR21CA176591 · NCI · JOHNS HOPKINS UNIVERSITY · PI XING, MICHAEL MINGZHAO · 2013 to 2014
$382k
NCI NIH HHS R01 CA113507NCI NIH HHS R01CA113507NCI NIH HHS R21 CA176591NCI NIH HHS R21CA176591
6 · The paper itself

Abstract

The role of the PI3K pathway in human cancer has been well established, but much of its molecular mechanism, particularly the epigenetic aspect, remains to be defined. We hypothesized that aberrant methylation and hence altered expression of certain unknown important genes induced by the genetically activated PI3K pathway signaling is a major epigenetic mechanism in human tumorigenesis. Through a genome-wide search for such genes that were epigenetically controlled by the PI3K pathway in thyroid cancer cells, we found a wide range of genes with broad functions epigenetically targeted by the PI3K pathway. The most prominent among these genes was REC8, classically known as a meiotic-specific gene, which we found to be robustly down-regulated by the PI3K pathway through hypermethylation. REC8 hypermethylation was strongly associated with genetic alterations and activities of the PI3K pathway in thyroid cancer cell lines, thyroid cancer tumors, and some other human cancers; it was also associated with poor clinicopathological outcomes of thyroid cancer, including advanced disease stages and patient mortality. Demethylating the hypermethylated REC8 gene restored its expression in thyroid cancer cells in which the PI3K pathway was genetically over-activated and induced expression of REC8 protein inhibited the proliferation and colony formation of these cells. These findings are consistent with REC8 being a novel major bona fide tumor suppressor gene and a robust epigenetic target of the PI3K pathway. Aberrant inactivation of REC8 through hypermethylation by the PI3K pathway may represent an important mechanism mediating the oncogenic functions of the PI3K pathway.

Indexed as

Cell Cycle ProteinsDNA MethylationEpigenesis, GeneticGene Expression ProfilingGenes, Tumor SuppressorGenome-Wide Association StudyHumansPhosphatidylinositol 3-KinasesReceptor, Adenosine A2BSignal TransductionThyroid NeoplasmsCell Cycle ProteinsPhosphatidylinositol 3-KinasesREC8 protein, humanReceptor, Adenosine A2BmethylationREC8thyroid cancerthyroid tumorigenesistumor suppressor gene

Identifiers

PMID26472282
PMCPMC4770767
OpenAlexW2254851952

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.