Evidence map›Paper›PMID 26083413›Full record

ArticlePloS one2015

Periostin Is a Key Niche Component for Wound Metastasis of Melanoma.

Keitaro Fukuda, Eiji Sugihara, Shoichiro Ohta, Kenji Izuhara, Takeru Funakoshi, Masayuki Amagai, Hideyuki Saya

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review of the premetastatic niche in liver cancer bone metastases.International journal of clinical and experimental pathology · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Periostin: biology and function in cancer.Cancer cell international · 2022
    Review
  8. Review
  9. Small extracellular vesicles in cancer.Bioactive materials · 2021
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Unraveling the ECM-Immune Cell Crosstalk in Skin Diseases.Frontiers in cell and developmental biology · 2019
    Review
  18. Review
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Keitaro FukudaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan; Department of Dermatology, Keio University School of Medicine, Tokyo, Japan.
Eiji SugiharaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Shoichiro OhtaDepartment of Laboratory Medicine, Saga Medical School, Saga, Japan.
Kenji IzuharaDivision of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.
Takeru FunakoshiDepartment of Dermatology, Keio University School of Medicine, Tokyo, Japan.
Masayuki AmagaiDepartment of Dermatology, Keio University School of Medicine, Tokyo, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Keio University · JPSaga Medical School Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue injury promotes metastasis of several human cancers, although factors associated with wound healing that attract circulating tumor cells have remained unknown. Here, we examined the primary and metastatic lesions that appeared 1 month after trauma in a patient with acral lentiginous melanoma. The levels of mRNA for periostin (POSTN), type 1 collagen, and fibronectin were significantly increased in the metastatic lesion relative to the primary lesion. The increase of these extracellular matrix proteins at the wound site was reproduced in a mouse model of wound healing, with the upregulation of Postn mRNA persisting the longest. POSTN was expressed in the region surrounding melanoma cell nests in metastatic lesions of both wounded mice and the patient. POSTN attenuated the cell adhesion and promoted the migration of melanoma cells without affecting their proliferation in vitro. In the mouse model, the wound site as well as subcutaneously injected osteoblasts that secrete large amounts of POSTN invited the metastasis of remotely-transplanted melanoma cells on the sites. Osteoblasts with suppression of POSTN by shRNA showed a greatly reduced ability to promote such metastasis. Our results suggest that POSTN is a key factor in promoting melanoma cell metastasis to wound sites by providing a premetastatic niche.

Indexed as

3T3 CellsAnimalsCell Adhesion MoleculesCell Line, TumorHumansMaleMelanomaMiceMice, Inbred BALB CMice, NudeMiddle AgedNeoplasm MetastasisSkinSkin NeoplasmsUp-RegulationWound HealingCell Adhesion MoleculesPOSTN protein, humanPostn protein, mouse

Identifiers

PMID26083413
PMCPMC4471156
OpenAlexW561543316

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.