Evidence map›Paper›PMID 22051193›Full record

ArticleDNA repair2012

Filamin-A as a marker and target for DNA damage based cancer therapy.

Jingyin Yue, Huimei Lu, Jingmei Liu, Marianne Berwick, Zhiyuan Shen

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2012. 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
1.5field-weighted citation impact, top 19% 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, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Exploring the Potential of Metal-Based Candidate Drugs as Modulators of the Cytoskeleton.Chembiochem : a European journal of chemical biology · 2023
    Review
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  5. Article
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  15. Article
  16. Inhibition of filamin-A reduces cancer metastatic potential.International journal of biological sciences · 2013
    Article
  17. Article
  18. Article
  19. Review
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

5 authors at 2 institutions in 1 country.

Jingyin YueDepartment of Radiation Oncology, The Cancer Institute of New Jersey, UMDNJ-Robert Wood Johnson Medical School, 195 Little Albany St., New Brunswick, NJ 08903, USA.
Huimei Lu
Jingmei Liu
Marianne Berwick
Zhiyuan Shen
Rutgers Cancer Institute of New JerseyUNM Comprehensive Cancer Center

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Alternative Mechanisms to Inactivate p53 During OncogenesisR01CA156706 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, ZHIYUAN · 2011 to 2015
$1.9M
Protection of Genomic Integrity by BCCIPR01CA115488 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI SHEN, ZHIYUAN · 2005 to 2009
$1.3M
NCI NIH HHS P30 CA072720NCI NIH HHS R01 CA115488NCI NIH HHS R01CA115488NCI NIH HHS R01 CA156706NCI NIH HHS R01CA156706
6 · The paper itself

Abstract

Filamin-A, also called actin binding protein 280 (ABP-280), cross-links the actin filaments into dynamic orthogonal network to serve as scaffolds in multiple signaling pathways. It has been reported that filamin-A interacts with DNA damage response proteins BRCA1 and BRCA2. Defects of filamin-A impair the repair of DNA double strand breaks (DSBs), resulting in sensitization of cells to ionizing radiation. In this study, we sought to test the hypothesis that filamin-A can be used as a target for cancer chemotherapy and as a biomarker to predict cancer response to therapeutic DNA damage. We found that reduction of filamin-A sensitizes cancer cells to chemotherapy reagents bleomycin and cisplatin, delays the repair of not only DSBs but also single strand breaks (SSBs) and interstrand crosslinks (ICLs), and increases chromosome breaks after the drug treatment. By treating a panel of human melanoma cell lines with variable filamin-A expression, we observed a correlation between expression level of filamin-A protein and drug IC(50). We further inhibited the expression of filamin-A in melanoma cells, and found that this confers an increased sensitivity to bleomycin and cisplatin treatment in a mouse xenograft tumor model. These results suggest that filamin-A plays a role in repair of a variety of DNA damage, that lack of filamin-A is a prognostic marker for a better outcome after DNA damage based treatment, and filamin-A can be inhibited to sensitize filamin-A positive cancer cells to therapeutic DNA damage. Thus filamin-A can be used as a biomarker and a target for DNA damage based cancer therapy.

Indexed as

DNA DamageAnimalsAntineoplastic AgentsBiomarkers, TumorBleomycinCell Line, TumorChromosomal InstabilityCisplatinContractile ProteinsDNA Breaks, Single-StrandedDNA RepairFilaminsGene Expression Regulation, NeoplasticHumansMelanomaMiceAntineoplastic AgentsBiomarkers, TumorBleomycinCisplatinContractile ProteinsFilaminsFLNC protein, humanMicrofilament Proteins

Identifiers

PMID22051193
PMCPMC3267325
OpenAlexW2055393058

What OpenQuestion holds

Textmetadata
LicenceTDM
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.