Evidence map›Paper›PMID 31667000›Full record

ArticleBone research2019

S100A4 released from highly bone-metastatic breast cancer cells plays a critical role in osteolysis.

Haemin Kim, Bongjun Kim, Sang Il Kim, Hyung Joon Kim, Brian Y Ryu, Junho Chung, Zang Hee Lee, Hong-Hee Kim

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Cell fusion in osteoclastogenesis.Biochemical Society transactions · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. The In Vivo Selection Method in Breast Cancer Metastasis.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Frontiers in pharmacology · 2020
    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

8 authors at 2 institutions in 1 country.

Haemin Kim *1Department of Cell and Developmental Biology, BK21 Program and DRI, Seoul National University, Seoul, Korea.
Bongjun Kim *1Department of Cell and Developmental Biology, BK21 Program and DRI, Seoul National University, Seoul, Korea.
Sang Il Kim2Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, Korea.
Hyung Joon Kim5Department of Oral Physiology, BK21 PLUS Project, and Dental and Life Science Institute, School of Dentistry, Pusan National University, Yangsan, Korea.
Brian Y Ryu6Interdisciplinary Program in Bioinformatics, Seoul National University College of Natural Sciences, Seoul, Korea.
Junho Chung2Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, Korea.
Zang Hee Lee1Department of Cell and Developmental Biology, BK21 Program and DRI, Seoul National University, Seoul, Korea.
Hong-Hee Kim1Department of Cell and Developmental Biology, BK21 Program and DRI, Seoul National University, Seoul, Korea.
Seoul National University · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone destruction induced by breast cancer metastasis causes severe complications, including death, in breast cancer patients. Communication between cancer cells and skeletal cells in metastatic bone microenvironments is a principal element that drives tumor progression and osteolysis. Tumor-derived factors play fundamental roles in this form of communication. To identify soluble factors released from cancer cells in bone metastasis, we established a highly bone-metastatic subline of MDA-MB-231 breast cancer cells. This subline (mtMDA) showed a markedly elevated ability to secrete S100A4 protein, which directly stimulated osteoclast formation via surface receptor RAGE. Recombinant S100A4 stimulated osteoclastogenesis in vitro and bone loss in vivo. Conditioned medium from mtMDA cells in which S100A4 was knocked down had a reduced ability to stimulate osteoclasts. Furthermore, the S100A4 knockdown cells elicited less bone destruction in mice than the control knockdown cells. In addition, administration of an anti-S100A4 monoclonal antibody (mAb) that we developed attenuated the stimulation of osteoclastogenesis and bone loss by mtMDA in mice. Taken together, our results suggest that S100A4 released from breast cancer cells is an important player in the osteolysis caused by breast cancer bone metastasis.

Indexed as

Bone cancerHomeostasis

Identifiers

PMID31667000
PMCPMC6804941
OpenAlexW2974855173

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.