Evidence map›Paper›PMID 21693594›Full record

ArticleMolecular cancer research : MCR2011

Downregulation of Filamin A interacting protein 1-like is associated with promoter methylation and induces an invasive phenotype in ovarian cancer.

Elizabeth R Burton, Aneesa Gaffar, Soo Jin Lee, Folashade Adeshuko, Kathleen D Whitney, Joon-Yong Chung, Stephen M Hewitt, Gloria S Huang, Gary L Goldberg, Steven K Libutti and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 29 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

11 authors at 5 institutions in 1 country.

Elizabeth R BurtonDepartment of Surgery, Albert Einstein College of Medicine of Yeshiva University, Bronx, NY 10461, USA.
Aneesa Gaffar
Soo Jin Lee
Folashade Adeshuko
Kathleen D Whitney
Joon-Yong Chung
Stephen M Hewitt
Gloria S Huang
Gary L Goldberg
Steven K Libutti
Mijung Kwon
Albert Einstein College of Medicine · USYeshiva University · USNational Cancer Institute · USCenter for Cancer Research · USMontefiore Medical Center · US

Funding

Tissue Array Research ProgramZICBC010923 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HEWITT, STEPHEN · 2009 to 2014
$4.7M
Intramural NIH HHS NIH0011496783Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecologic malignancy with a five-year survival rate below 25% for patients with stages III and IV disease. Identifying key mediators of ovarian cancer invasion and metastasis is critical to the development of more effective therapeutic interventions. We previously identified Filamin A interacting protein 1-like (FILIP1L) as an important mediator of cell proliferation and migration. In addition, targeted expression of FILIP1L in tumors inhibited tumor growth in vivo. In our present study, we confirmed that both mRNA and protein expression of FILIP1L were downregulated in ovarian cancer cells compared with normal ovarian epithelial cells. FILIP1L expression was inversely correlated with the invasive potential of ovarian cancer cell lines and clinical ovarian cancer specimens. We also provide evidence that DNA methylation is a mechanism by which FILIP1L is downregulated in ovarian cancer. The CpG island in the FILIP1L promoter was heavily methylated in ovarian cancer cells. Methylation status of the FILIP1L promoter was inversely correlated with FILIP1L expression in ovarian cell lines and clinical ovarian specimens. Reduced methylation in the FILIP1L promoter following treatment with a DNA demethylating agent was associated with restoration of FILIP1L expression in ovarian cancer cells. A transcription activator, cAMP-responsive element binding protein (CREB) was shown to bind to the CREB/ATF site in the CpG island of the FILIP1L promoter. Overall, these findings suggest that downregulation of FILIP1L associated with DNA methylation is related with the invasive phenotype in ovarian cancer and that modulation of FILIP1L expression has the potential to be a target for ovarian cancer therapy.

Indexed as

Gene Expression Regulation, NeoplasticCarrier ProteinsCell LineCell Line, TumorCell MovementCell ProliferationCpG IslandsCyclic AMP Response Element-Binding ProteinCytoskeletal ProteinsDNA MethylationFemaleHumansNeoplasm InvasivenessNeoplasm StagingOvarian NeoplasmsPhenotypeCarrier ProteinsCREB1 protein, humanCyclic AMP Response Element-Binding ProteinCytoskeletal ProteinsFILIP1 protein, human

Identifiers

PMID21693594
PMCPMC3157597
OpenAlexW2118479487

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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.