Evidence map›Paper›PMID 32272947›Full record

ArticleBreast cancer research : BCR2020

Breast cancer bone metastases are attenuated in a Tgif1-deficient bone microenvironment.

Marie-Therese Haider, Hiroaki Saito, Jennifer Zarrer, Kevin Uzhunnumpuram, Sankari Nagarajan, Vijayalakshmi Kari, Michael Horn-Glander, Stefan Werner, Eric Hesse, Hanna Taipaleenmäki

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

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  9. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
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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

10 authors at 6 institutions in 2 countries.

Marie-Therese HaiderMolecular Skeletal Biology Laboratory, Department of Trauma, Hand and Reconstructive Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hiroaki SaitoInstitute of Molecular Musculoskeletal Research, University Hospital, LMU Munich, Munich, Germany.
Jennifer ZarrerMolecular Skeletal Biology Laboratory, Department of Trauma, Hand and Reconstructive Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Kevin UzhunnumpuramMolecular Skeletal Biology Laboratory, Department of Trauma, Hand and Reconstructive Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sankari NagarajanDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen Center for Molecular Biosciences, Göttingen, Germany.
Vijayalakshmi KariDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen Center for Molecular Biosciences, Göttingen, Germany.
Michael Horn-GlanderUniversity Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Stefan WernerInstitute of Tumor Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Eric HesseInstitute of Molecular Musculoskeletal Research, University Hospital, LMU Munich, Munich, Germany.
Hanna TaipaleenmäkiMolecular Skeletal Biology Laboratory, Department of Trauma, Hand and Reconstructive Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. h.taipaleenmaeki@uke.de.
Universität Hamburg · DELMU Klinikum · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversitätsmedizin Göttingen · DEUniversity Cancer Center Hamburg · DEUniversity of Cambridge · GB

Funding

Alexander von Humboldt-Stiftung (DE) Post-doctoral FellowshipBundesministerium für Bildung und Forschung 01KU1401BDeutsche Forschungsgemeinschaft HE 5208/2-1, HE 5208/2-3, HE 5208/5-1Deutsche Forschungsgemeinschaft TA 1154/1-1, TA 1154/2-1
6 · The paper itself

Abstract

backgroundOsteoclast activation is a hallmark of breast cancer-induced bone disease while little is known about the role of osteoblasts in this process. Recently, we identified the homeodomain protein TG-interacting factor-1 (Tgif1) as a crucial regulator of osteoblast function. In this study, we demonstrate that lack of Tgif1 also restricts the progression of breast cancer bone metastases.

methodsTranswell migration assays were used to investigate the osteoblast-breast cancer cell interaction in vitro. Molecular analyses included RNA sequencing, immunoblotting, and qRT-PCR. To determine the role of Tgif1 in metastatic bone disease, 4T1 breast cancer cells were injected intracardially into mice with a germ line deletion of Tgif1 (Tgif1

resultsMedium conditioned by osteoblasts stimulated breast cancer cell migration, indicating a potential role of osteoblasts during bone metastasis progression. Tgif1 expression was strongly increased in osteoblasts upon stimulation by breast cancer cells, demonstrating the implication of Tgif1 in the osteoblast-breast cancer cell interaction. Indeed, conditioned medium from osteoblasts of Tgif1

conclusionWe propose that the lack of Tgif1 in osteoblasts increases Sema3E expression and attenuates breast cancer cell migration as well as metastases formation.

Indexed as

Tumor MicroenvironmentAnimalsBone and BonesBone NeoplasmsBreast NeoplasmsCell DifferentiationCell Line, TumorDisease Models, AnimalFemaleHomeodomain ProteinsHumansMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutOsteoblastsHomeodomain ProteinsRepressor ProteinsSEMA3E protein, humanSemaphorinsTGIF1 protein, humanTgif1 protein, mouseBone metastasesBreast cancerOsteoblastsTgif1

Identifiers

PMID32272947
PMCPMC7146874
OpenAlexW3015360868

What OpenQuestion holds

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LicenceCC BY
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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.