Evidence map›Paper›PMID 26838548›Full record

ArticleScience signaling2016

ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling.

Jun Wang, Clay Rouse, Jeff S Jasper, Ann Marie Pendergast

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Genomic and immune profiling of breast cancer brain metastases.Acta neuropathologica communications · 2025
    Article
  4. Acetylation and Deacetylation of Cytoskeleton-Associated Proteins.Results and problems in cell differentiation · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. ABL kinases regulate the stabilization of HIF-1α and MYC through CPSF1.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Review
  11. Review
  12. Article
  13. Article
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  15. Article
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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

4 authors at 1 institution in 1 country.

Jun WangDepartment of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA.
Clay RouseDivision of Laboratory Animal Resources, Duke University School of Medicine, Durham, NC 27710, USA.
Jeff S JasperDepartment of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA.
Ann Marie PendergastDepartment of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC 27710, USA. ann.pendergast@duke.edu.
Duke University · US

Funding

Duke CTSA (Composite)UL1TR001117 · NCATS · DUKE UNIVERSITY · PI BOULWARE, LEIGH E, LI, JENNIFER S · 2013 to 2017
$41.3M
The role of ERRalpha/PGC-1 in disease pathogenesisR01CA174643 · NCI · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 2013 to 2017
$1.6M
Kinase Target of Diverse Cell Surface Receptors in Cancer Invasion and MetastasisR01CA155160 · NCI · DUKE UNIVERSITY · PI PENDERGAST, ANN MARIE · 2011 to 2015
$1.6M
NCATS NIH HHS UL1 TR001117NCATS NIH HHS UL1TR001117NCI NIH HHS CA174643NCI NIH HHS R01 CA155160NCI NIH HHS R01 CA174643
6 · The paper itself

Abstract

Bone metastases occur in up to 70% of advanced breast cancer. For most patients with breast cancer, bone metastases are predominantly osteolytic. Interactions between tumor cells and stromal cells in the bone microenvironment drive osteolytic bone metastasis, a process that requires the activation of osteoclasts, cells that break down bone. We report that ABL kinases promoted metastasis of breast cancer cells to bone by regulating the crosstalk between tumor cells and the bone microenvironment. ABL kinases protected tumor cells from apoptosis induced by TRAIL (TNF-related apoptosis-inducing ligand), activated the transcription factor STAT5, and promoted osteolysis through the STAT5-dependent expression of genes encoding the osteoclast-activating factors interleukin-6 (IL-6) and matrix metalloproteinase 1 (MMP1). Furthermore, in breast cancer cells, ABL kinases increased the abundance of the Hippo pathway mediator TAZ and the expression of TAZ-dependent target genes that promote bone metastasis. Knockdown of ABL kinases or treatment with ABL-specific allosteric inhibitor impaired osteolytic metastasis of breast cancer cells in mice. These findings revealed a role for ABL kinases in regulating tumor-bone interactions and provide a rationale for using ABL-specific inhibitors to limit breast cancer metastasis to bone.

Indexed as

Signal TransductionAnimalsBone NeoplasmsBreast NeoplasmsCell Line, TumorFemaleHeterograftsHumansIntracellular Signaling Peptides and ProteinsMiceMice, NudeNeoplasm MetastasisNeoplasm TransplantationOsteolysisProto-Oncogene Proteins c-ablSTAT5 Transcription FactorIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-ablSTAT5 Transcription FactorTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, human

Identifiers

PMID26838548
PMCPMC4991033
OpenAlexW2273321144

What OpenQuestion holds

Textmetadata
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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.