Evidence map›Paper›PMID 26320173›Full record

ArticleOncotarget2015

RUNX2 and TAZ-dependent signaling pathways regulate soluble E-Cadherin levels and tumorsphere formation in breast cancer cells.

Jessica L Brusgard, Moran Choe, Saranya Chumsri, Keli Renoud, Alexander D MacKerell, Marius Sudol, Antonino Passaniti

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Runt-related transcription factors in human carcinogenesis: a friend or foe?Journal of cancer research and clinical oncology · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. An overview of signaling pathways regulating YAP/TAZ activity.Cellular and molecular life sciences : CMLS · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 4 institutions in 2 countries.

Jessica L BrusgardProgram in Molecular Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Moran ChoeGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Saranya ChumsriDepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Keli RenoudGreenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Alexander D MacKerellDepartment of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, MD, USA.
Marius SudolMechanobiology Institute, Department of Physiology, National University of Singapore, Singapore.
Antonino PassanitiDepartment of Pathology and Department of Biochemistry & Molecular Biology, The Marlene & Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
University of Maryland, Baltimore · USNational University of Singapore · SGU-M Rogel Cancer CenterUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center

Funding

Transcriptional regulation of tumor growthI01BX002205 · VA · BALTIMORE VA MEDICAL CENTER · PI PASSANITI, ANTONINO · 2014 to 2017
–
BLRD VA I01 BX002205
6 · The paper itself

Abstract

Intratumoral heterogeneity and treatment resistance drive breast cancer (BC) metastasis and recurrence. The RUNX2 transcription factor is upregulated in early stage luminal BC. However, the precise mechanism by which RUNX2 regulates an oncogenic phenotype in luminal BCs remains an enigma. We show that RUNX2 is predictive of poor overall survival in BC patients. RUNX2 associated with the TAZ transcriptional co-activator to promote a tumorigenic phenotype that was inhibited by knockdown of TAZ. RUNX2 increased endogenous TAZ translocation to the nucleus, which was prevented by inhibiting RUNX2. RUNX2/TAZ interaction was associated with ectodomain shedding of an oncogenic soluble E-Cadherin fragment (sE-Cad), which is known to cooperate with human epidermal growth factor receptor-2 (HER2/ErbB2) to increase BC growth. Neutralizing E-Cadherin antibodies or TAZ knockdown reduced the levels of sE-Cad in RUNX2-expressing BC cells and inhibited tumorsphere formation. RUNX2 expression also increased HER2-mediated tumorsphere size, which was reduced after treatment with the HER2-targeting agents Herceptin and lapatinib. These data support a novel role for RUNX2 in promoting an oncogenic phenotype in luminal BC in the context of TAZ, sE-Cad, and HER2. Using this signaling pathway to monitor BC cell oncogenic activity will accelerate the discovery of new therapeutic modalities to treat BC patients.

Indexed as

Signal TransductionAnimalsBlotting, WesternBreast NeoplasmsCadherinsCore Binding Factor Alpha 1 SubunitDoxycyclineErb-b2 Receptor Tyrosine KinasesGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMCF-7 CellsMiceNIH 3T3 CellsProtein BindingReverse Transcriptase Polymerase Chain ReactionCadherinsCore Binding Factor Alpha 1 SubunitDoxycyclineErb-b2 Receptor Tyrosine KinasesIntracellular Signaling Peptides and ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanbreast cancertherapeuticstranscription factorstumorspheres

Identifiers

PMID26320173
PMCPMC4695049
OpenAlexW1256678445

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.