Evidence map›Paper›PMID 29759731›Full record

ArticleBiomaterials2019

Intrafibrillar, bone-mimetic collagen mineralization regulates breast cancer cell adhesion and migration.

Siyoung Choi, Jens Friedrichs, Young Hye Song, Carsten Werner, Lara A Estroff, Claudia Fischbach

Abstract read
In one paragraph

Article in Biomaterials, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 76 citations in OpenAlex.

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  3. Mitochondrial transfer in the HSC-HCC-macrophage network shapes hepatocellular carcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

6 authors at 2 institutions in 2 countries.

Siyoung ChoiNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY 14853, USA.
Jens FriedrichsInstitute of Biofunctional Polymer Materials, Leibniz Institute of Polymer Research Dresden, 01069 Dresden, Germany.
Young Hye SongNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY 14853, USA.
Carsten WernerInstitute of Biofunctional Polymer Materials, Leibniz Institute of Polymer Research Dresden, 01069 Dresden, Germany.
Lara A EstroffDepartment of Materials Science and Engineering, Cornell University, Ithaca, NY 14853, USA; Kavli Institute at Cornell for Nanoscale Science, Cornell University, Ithaca, NY 14853, USA. Electronic address: lae37@cornell.edu.
Claudia FischbachNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY 14853, USA; Kavli Institute at Cornell for Nanoscale Science, Cornell University, Ithaca, NY 14853, USA. Electronic address: cf99@cornell.edu.
Cornell University · USLeibniz Institute of Polymer Research · DE

Funding

Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI SCHAFFER, CHRIS B · 2016 to 2020
$10.2M
Breast microcalcifications and their role in breast cancer bone metastasisR01CA173083 · NCI · CORNELL UNIVERSITY · PI FISCHBACH, CLAUDIA · 2012 to 2016
$1.7M
UltraVIEW VoX spinning disk confocal for core facilityS10OD010605 · OD · CORNELL UNIVERSITY · PI WILLIAMS, REBECCA M · 2012 to 2012
$595k
Zeiss LSM710 Confocal Microscope for Shared Imaging FacilityS10RR025502 · NCRR · CORNELL UNIVERSITY · PI WILLIAMS, REBECCA M · 2009 to 2009
$500k
NCI NIH HHS R01 CA173083NCI NIH HHS U54 CA210184NCRR NIH HHS S10 RR025502NIH HHS S10 OD010605
6 · The paper itself

Abstract

Bone metastasis is a leading cause of death in patients with breast cancer, but the underlying mechanisms are poorly understood. While much work focuses on the molecular and cellular events that drive breast cancer bone metastasis, it is mostly unclear what role bone extracellular matrix (ECM) properties play in this process. Bone ECM primarily consists of mineralized collagen fibrils, which are composed of non-stoichiometric carbonated apatite (HA) and collagen type I. Reduced bone mineral content is epidemiologically linked with increased risk of bone metastasis. Yet elucidating the potential functional impact of collagen mineralization on breast cancer cells has remained challenging because of a lack of model systems that allow studying tumor cell behavior as a function of physiological, intrafibrillar collagen mineralization. Here, we have developed cell culture substrates composed of mineralized collagen type I fibrils using a polymer-induced liquid-precursor (PILP) process. Intrafibrillar HA decreased breast cancer cell adhesion forces and accordingly reduced collagen fiber alignment relative to cells cultured on control collagen. The resulting mineral-mediated changes in collagen network characteristics and mechanosignaling correlated with increased cell motility, but inhibited directed migration of breast cancer cells. These results suggest that physiological mineralization of collagen fibrils reduces tumor cell adhesion with potential functional consequences on skeletal homing of disseminated tumor cells in early stages of breast cancer metastasis.

Indexed as

AnimalsApatitesBiocompatible MaterialsBiomechanical PhenomenaBone NeoplasmsBreast NeoplasmsCalcification, PhysiologicCell AdhesionCell Line, TumorCell MovementCollagen Type IElastic ModulusFemaleHumansRatsApatitesBiocompatible MaterialsCollagen Type IBone metastasisCollagen fiber alignmentHydroxyapatiteIntrafibrillar collagen mineralizationMechanosignaling

Identifiers

PMID29759731
PMCPMC6222013
OpenAlexW2802819154

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.