Evidence map›Paper›PMID 25868708›Full record

ArticleInternational journal of cancer2015

Transcriptional regulation of tenascin-W by TGF-beta signaling in the bone metastatic niche of breast cancer cells.

Francesca Chiovaro, Enrico Martina, Alessia Bottos, Arnaud Scherberich, Nancy E Hynes, Ruth Chiquet-Ehrismann

Open access · hybridAbstract read
In one paragraph

Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Exploring bone-tumor interactions through 3DJournal of bone oncology · 2025
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  10. The extracellular matrix in tumor progression and metastasis.Clinical & experimental metastasis · 2019
    Review
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  20. Matricellular proteins as regulators of cancer metastasis to bone.Matrix biology : journal of the International Society for Matrix Biology
    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

6 authors at 3 institutions in 1 country.

Francesca ChiovaroFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Enrico MartinaFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Alessia BottosFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Arnaud ScherberichDepartment of Biomedicine, University Hospital Basel, Basel, Switzerland.
Nancy E HynesFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Ruth Chiquet-EhrismannFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Friedrich Miescher Institute · CHUniversity of Basel · CHUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-W is a matricellular protein with a dynamically changing expression pattern in development and disease. In adults, tenascin-W is mostly restricted to stem cell niches, and is also expressed in the stroma of solid cancers. Here, we analyzed its expression in the bone microenvironment of breast cancer metastasis. Osteoblasts were isolated from tumor-free or tumor-bearing bones of mice injected with MDA-MB231-1833 breast cancer cells. We found a fourfold upregulation of tenascin-W in the osteoblast population of tumor-bearing mice compared to healthy mice, indicating that tenascin-W is supplied by the bone metastatic niche. Transwell and co-culture studies showed that human bone marrow stromal cells (BMSCs) express tenascin-W protein after exposure to factors secreted by MDA-MB231-1833 breast cancer cells. To study tenascin-W gene regulation, we identified and analyzed the tenascin-W promoter as well as three evolutionary conserved regions in the first intron. 5'RACE analysis of mRNA from human breast cancer, glioblastoma and bone tissue showed a single tenascin-W transcript with a transcription start site at a noncoding first exon followed by exon 2 containing the ATG translation start. Site-directed mutagenesis of a SMAD4-binding element in proximity of the TATA box strongly impaired promoter activity. TGFβ1 induced tenascin-W expression in human BMSCs through activation of the TGFβ1 receptor ALK5, while glucocorticoids were inhibitory. Our experiments show that tenascin-W acts as a niche component for breast cancer metastasis to bone by supporting cell migration and cell proliferation of the cancer cells.

Indexed as

AnimalsBone Marrow CellsBone NeoplasmsBreast NeoplasmsCell Line, TumorCell ProliferationCoculture TechniquesFemaleHumansMiceNeoplasm TransplantationOsteoblastsSignal TransductionStromal CellsTenascinTransforming Growth Factor betaTenascintenascin-N protein, mousetenascin-W, humanTransforming Growth Factor betabonebreast cancergene regulationmetastatic nichetenascin

Identifiers

PMID25868708
PMCPMC5029769
OpenAlexW1512489780

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.