Evidence map›Paper›PMID 21209904›Full record

ArticlePloS one2010

Therapeutic implications of GIPC1 silencing in cancer.

Thomas W Chittenden, Jane Pak, Renee Rubio, Hailing Cheng, Kristina Holton, Niall Prendergast, Vladimir Glinskii, Yi Cai, Aedin Culhane, Stefan Bentink and 12 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

24 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. The Role of Rho GTPases in VEGF Signaling in Cancer Cells.Analytical cellular pathology (Amsterdam) · 2020
    Review
  12. Article
  13. Emerging Themes in PDZ Domain Signaling: Structure, Function, and Inhibition.International review of cell and molecular biology · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

22 authors at 7 institutions in 3 countries.

Thomas W ChittendenFunctional Genomics and Computational Biology Group, Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States America.
Jane Pak
Renee Rubio
Hailing Cheng
Kristina Holton
Niall Prendergast
Vladimir Glinskii
Yi Cai
Aedin Culhane
Stefan Bentink
Mathew Schwede
Jessica C Mar
Eleanor A Howe
Martin Aryee
Razvan Sultana
Anthony A Lanahan
Jennifer M Taylor
Chris Holmes
William C Hahn
Jean J Zhao
J Dirk Iglehart
John Quackenbush
Dana-Farber Cancer Institute · USHarvard University · USCommonwealth Scientific and Industrial Research Organisation · AUMassachusetts Institute of Technology · USSidney Kimmel Comprehensive Cancer Center · USUniversity of Oxford · GBYale University · US

Funding

Roles of class 1A PI3K isoforms in mammary epithelium function and breast cancerR01CA134502 · NCI · DANA-FARBER CANCER INST · PI ZHAO, JEAN · 2008 to 2012
$1.7M
Integrated approaches to deriving predictive networks from public data sourcesR01LM010129 · NLM · DANA-FARBER CANCER INST · PI QUACKENBUSH, JOHN · 2009 to 2010
$1.4M
Medical Research Council G0500115Medical Research Council MC_UP_A390_1107NLM NIH HHS R01 LM010129NLM NIH HHS R01LM010129
6 · The paper itself

Abstract

GIPC1 is a cytoplasmic scaffold protein that interacts with numerous receptor signaling complexes, and emerging evidence suggests that it plays a role in tumorigenesis. GIPC1 is highly expressed in a number of human malignancies, including breast, ovarian, gastric, and pancreatic cancers. Suppression of GIPC1 in human pancreatic cancer cells inhibits in vivo tumor growth in immunodeficient mice. To better understand GIPC1 function, we suppressed its expression in human breast and colorectal cancer cell lines and human mammary epithelial cells (HMECs) and assayed both gene expression and cellular phenotype. Suppression of GIPC1 promotes apoptosis in MCF-7, MDA-MD231, SKBR-3, SW480, and SW620 cells and impairs anchorage-independent colony formation of HMECs. These observations indicate GIPC1 plays an essential role in oncogenic transformation, and its expression is necessary for the survival of human breast and colorectal cancer cells. Additionally, a GIPC1 knock-down gene signature was used to interrogate publically available breast and ovarian cancer microarray datasets. This GIPC1 signature statistically correlates with a number of breast and ovarian cancer phenotypes and clinical outcomes, including patient survival. Taken together, these data indicate that GIPC1 inhibition may represent a new target for therapeutic development for the treatment of human cancers.

Indexed as

ApoptosisGene Expression Regulation, NeoplasticGene SilencingAdaptor Proteins, Signal TransducingAntineoplastic AgentsBreast NeoplasmsCell Transformation, NeoplasticColorectal NeoplasmsDisease ProgressionEpithelial CellsFemaleHumansOligonucleotide Array Sequence AnalysisPolymerase Chain ReactionRNA InterferenceAdaptor Proteins, Signal TransducingAntineoplastic AgentsGIPC1 protein, human

Identifiers

PMID21209904
PMCPMC3012716
OpenAlexW2119050497

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.