Evidence map›Paper›PMID 33549040›Full record

ArticleBMC cancer2021

The role of S100A4 for bone metastasis in prostate cancer cells.

Bongjun Kim, Suhan Jung, Haemin Kim, Jun-Oh Kwon, Min-Kyoung Song, Min Kyung Kim, Hyung Joon Kim, Hong-Hee Kim

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2021. 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
1.5field-weighted citation impact, top 17% 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, 27 citations in OpenAlex.

  1. Review
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  10. ACS applied materials & interfaces · 2024
    Article
  11. Observational
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  14. Article
  15. Follow-Up Biomarkers in the Evolution of Prostate Cancer, Levels ofInternational journal of molecular sciences · 2022
    Article
  16. Article
  17. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  18. S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  19. Review
  20. 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

8 authors at 3 institutions in 3 countries.

Bongjun Kim *Department of Cell and Developmental Biology, BK21 PLUS Program and DRI, School of Dentistry, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea, 03080.
Suhan Jung *Department of Cell and Developmental Biology, BK21 PLUS Program and DRI, School of Dentistry, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea, 03080.
Haemin KimArthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York City, NY, USA.
Jun-Oh KwonDepartment of Cell and Developmental Biology, BK21 PLUS Program and DRI, School of Dentistry, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea, 03080.
Min-Kyoung SongDepartment of Cell and Developmental Biology, BK21 PLUS Program and DRI, School of Dentistry, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea, 03080.
Min Kyung KimDepartment of Cell and Developmental Biology, BK21 PLUS Program and DRI, School of Dentistry, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea, 03080.
Hyung Joon KimDepartment of Oral Physiology, BK21 PLUS Project, and Dental and Life Science Institute, School of Dentistry, Pusan National University, Mulgeum-eup, Yangsan, Busan, 50612, South Korea.
Hong-Hee KimDepartment of Cell and Developmental Biology, BK21 PLUS Program and DRI, School of Dentistry, Seoul National University, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea, 03080. hhbkim@snu.ac.kr.ORCID http://orcid.org/0000-0002-1411-6106
Seoul National University · KRHospital for Special Surgery · USThe University of Texas MD Anderson Cancer Center · US

Funding

National Research Foundation of Korea NRF-2018R1A5A2024418National Research Foundation of Korea NRF-2019R1A2C4070083National Research Foundation of Korea NRF-2020R1A2C2010082
6 · The paper itself

Abstract

backgroundProstate cancers frequently metastasize to bone, where the best microenvironment for distant colonization is provided. Since osteotropic metastasis of prostate cancer is a critical determinant of patients' survival, searches for preventive measures are ongoing in the field. Therefore, it is important to dissect the mechanisms of each step of bone metastasis, including the epithelial-mesenchymal transition (EMT) and cross-talk between metastatic niches and cancer cells.

methodsIn this study, we established a highly bone-metastatic subline of human prostate cancer cells by selecting bone-homing population of PC3 cells after cardiac injection of eight-week-old male BALB/c-nude mice. Then we assessed the proliferation, EMT characteristics, and migration properties of the subline (mtPC3) cells in comparison with the parental PC3 cells. To investigate the role of S100A4, we performed gene knock-down by lentiviral transduction, or treated cells with recombinant S100A4 protein or a S100A4-neutralizing antibody. The effect of cancer cells on osteoclastogenesis was evaluated after treatment of pre-osteoclasts with conditioned medium (CM) from cancer cells.

resultsThe mtPC3 cells secreted a markedly high level of S100A4 protein and showed elevated cell proliferation and mesenchymal properties. The increased proliferation and EMT traits of mtPC3 cells was inhibited by S100A4 knock-down, but was not affected by exogenous S100A4. Furthermore, S100A4 released from mtPC3 cells stimulated osteoclast development via the cell surface receptor RAGE. Down-regulation or neutralization of S100A4 in the CM of mtPC3 cells attenuated cancer-induced osteoclastogenesis.

conclusionAltogether, our results suggest that intracellular S100A4 promotes cell proliferation and EMT characteristics in tumor cells, and that secreted S100A4 activates osteoclastogenesis, contributing to osteolytic bone metastasis. Thus, S100A4 upregulation in cancer cells highly metastatic to bone might be a key element in regulating bone metastasis.

Indexed as

Cell ProliferationEpithelial-Mesenchymal TransitionAnimalsBone NeoplasmsCell CommunicationCell DifferentiationCell MovementCulture Media, ConditionedDown-RegulationHumansMaleMiceMice, Inbred BALB CMice, Inbred ICRMice, NudeOsteoclastsCulture Media, ConditionedS100 Calcium-Binding Protein A4Bone metastasisEpithelial-mesenchymal transitionOsteoclastProstate cancerS100A4

Identifiers

PMID33549040
PMCPMC7868026
OpenAlexW3126705809

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.