Evidence map›Paper›PMID 22964639›Full record

ArticleOncogene2013

Inhibition of metastasis by HEXIM1 through effects on cell invasion and angiogenesis.

W Ketchart, K M Smith, T Krupka, B M Wittmann, Y Hu, P A Rayman, Y Q Doughman, J M Albert, X Bai, J H Finke and 3 more

Abstract read
In one paragraph

Article in Oncogene, 2013. 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
0.9field-weighted citation impact, top 24% 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, 35 citations in OpenAlex.

  1. cGAS/STING-Independent Induction of Type I Interferon by Inhibitors of the Histone Methylase KDM5B.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  7. CoMM-SFrontiers in genetics · 2021
    Article
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  13. Review
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  17. Review
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  20. Lead optimization of HMBA to develop potent HEXIM1 inducers.Bioorganic & medicinal chemistry letters · 2014
    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

13 authors at 3 institutions in 2 countries.

W KetchartDepartment of Pharmacology, Case Western Reserve University Cleveland, Cleveland, OH, USA.
K M Smith
T Krupka
B M Wittmann
Y Hu
P A Rayman
Y Q Doughman
J M Albert
X Bai
J H Finke
Y Xu
A A Exner
M M Montano
Case Western Reserve University · USCleveland Clinic Lerner College of Medicine · USCleveland State University · US

Funding

A Novel Growth Regulatory Factor in Breast CellsR01CA092440 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MONTANO, MONICA · 2002 to 2012
$3.0M
Functional Polymer Matrixes for Site-Specific, Image Guided Drug DeliveryR01CA118399 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI EXNER, AGATA A · 2006 to 2010
$1.5M
NCI NIH HHS CA92440NCI NIH HHS R01 CA092440NCI NIH HHS R01 CA118399NCI NIH HHS R01CA118399
6 · The paper itself

Abstract

We report on the role of hexamethylene-bis-acetamide-inducible protein 1 (HEXIM1) as an inhibitor of metastasis. HEXIM1 expression is decreased in human metastatic breast cancers when compared with matched primary breast tumors. Similarly we observed decreased expression of HEXIM1 in lung metastasis when compared with primary mammary tumors in a mouse model of metastatic breast cancer, the polyoma middle T antigen (PyMT) transgenic mouse. Re-expression of HEXIM1 (through transgene expression or localized delivery of a small molecule inducer of HEXIM1 expression, hexamethylene-bis-acetamide) in PyMT mice resulted in inhibition of metastasis to the lung. Our present studies indicate that HEXIM1 downregulation of HIF(-)1α protein allows not only for inhibition of vascular endothelial growth factor-regulated angiogenesis, but also for inhibition of compensatory pro-angiogenic pathways and recruitment of bone marrow-derived cells (BMDCs). Another novel finding is that HEXIM1 inhibits cell migration and invasion that can be partly attributed to decreased membrane localization of the 67 kDa laminin receptor, 67LR, and inhibition of the functional interaction of 67LR with laminin. Thus, HEXIM1 re-expression in breast cancer has therapeutic advantages by simultaneously targeting more than one pathway involved in angiogenesis and metastasis. Our results also support the potential for HEXIM1 to indirectly act on multiple cell types to suppress metastatic cancer.

Indexed as

AnimalsBlotting, WesternChromatography, High Pressure LiquidFemaleFlow CytometryHumansHypoxia-Inducible Factor 1, alpha SubunitImmunohistochemistryImmunoprecipitationLung NeoplasmsMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, TransgenicNeoplasm InvasivenessNeovascularization, PathologicHexim1 protein, mouseHypoxia-Inducible Factor 1, alpha SubunitRNA-Binding ProteinsTranscription Factors

Identifiers

PMID22964639
PMCPMC3525740
OpenAlexW2101370689

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.