Evidence map›Paper›PMID 25205099›Full record

ArticleCancer research2014

Histone h1.3 suppresses h19 noncoding RNA expression and cell growth of ovarian cancer cells.

Magdalena Medrzycki, Yunzhe Zhang, Weijia Zhang, Kaixiang Cao, Chenyi Pan, Nathalie Lailler, John F McDonald, Eric E Bouhassira, Yuhong Fan

Abstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Magdalena MedrzyckiSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia. The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia.
Yunzhe ZhangSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia. The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia.
Weijia ZhangDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York.
Kaixiang CaoSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia. The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia.
Chenyi PanSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia. The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia.
Nathalie LaillerMemorial Sloan-Kettering Cancer Center, New York.
John F McDonaldSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia. The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia.
Eric E BouhassiraDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, New York.
Yuhong FanSchool of Biology, Georgia Institute of Technology, Atlanta, Georgia. The Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia. Yuhong.fan@biology.gatech.edu.
Georgia Institute of Technology · USAlbert Einstein College of Medicine · USIcahn School of Medicine at Mount Sinai · USKettering University · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
Role of Linker Histone H1 in Epigenetic Gene RegulationR01GM085261 · NIGMS · GEORGIA INSTITUTE OF TECHNOLOGY · PI FAN, YUHONG · 2008 to 2012
$2.0M
NCI NIH HHS P30 CA013330NIGMS NIH HHS GM085261NIGMS NIH HHS R01 GM085261
6 · The paper itself

Abstract

Ovarian cancer is a deadly gynecologic malignancy for which novel biomarkers and therapeutic targets are imperative for improving survival. Previous studies have suggested the expression pattern of linker histone variants as potential biomarkers for ovarian cancer. To investigate the role of histone H1 in ovarian cancer cells, we characterize individual H1 variants and overexpress one of the major somatic H1 variants, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line. We find that overexpression of H1.3 decreases the growth rate and colony formation of OVCAR-3 cells. We identify histone H1.3 as a specific repressor for the noncoding oncogene H19. Overexpression of H1.3 suppresses H19 expression, and knockdown of H1.3 increases its expression in multiple ovarian epithelial cancer cell lines. Furthermore, we demonstrate that histone H1.3 overexpression leads to increased occupancy of H1.3 at the H19 regulator region encompassing the imprinting control region (ICR), concomitant with increased DNA methylation and reduced occupancy of the insulator protein CTCF at the ICR. Finally, we demonstrate that H1.3 overexpression and H19 knockdown synergistically decrease the growth rate of ovarian cancer cells. Our findings suggest that H1.3 dramatically inhibits H19 expression, which contributes to the suppression of epithelial ovarian carcinogenesis.

Indexed as

Cell ProliferationCell Line, TumorDNA MethylationFemaleGene Expression Regulation, NeoplasticHistonesHumansOvarian NeoplasmsRNA, Long NoncodingH19 long non-coding RNAHistonesRNA, Long Noncoding

Identifiers

PMID25205099
PMCPMC4233163
OpenAlexW2077937417

What OpenQuestion holds

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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.