Evidence map›Paper›PMID 39581861›Full record

ReviewCancer science2025

S100A8 as a potential therapeutic target for cancer metastasis.

Atsuko Deguchi, Yoshiro Maru

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

2 authors.

Atsuko DeguchiInstitute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, Tokyo, Japan.ORCID https://orcid.org/0000-0001-9647-3539
Yoshiro MaruDepartment of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.

Funding

Japan Society for the Promotion of Science JP21K07157Japan Society for the Promotion of Science JP24K10364
6 · The paper itself

Abstract

Metastasis is a major cause of cancer-related deaths. Similar to the tumor microenvironment formation, the premetastatic niche develops in distant organs before the arrival of tumor cells. Elucidating the mechanism(s) underlying premetastatic niche formation could contribute to the establishment of effective therapeutic targets for metastasis. Our research indicates that primary tumors hijack Toll-like receptor 4 (TLR4) signaling to establish a premetastatic niche in the lungs by utilizing an endogenous ligand S100A8. S100A8 is expressed not only in immune cells but also in various types of tumor cells. By focusing on S100A8 as a therapeutic target, we identified at least three multivalent S100A8 inhibitory peptides. Here, we review the tumor-promoting role of S100A8-mediated TLR4 signaling and propose S100A8 as a potential therapeutic target for aggressive cancer.

Indexed as

Calgranulin ANeoplasm MetastasisNeoplasmsAnimalsHumansMolecular Targeted TherapySignal TransductionToll-Like Receptor 4Tumor MicroenvironmentCalgranulin AS100A8 protein, humanTLR4 protein, humanToll-Like Receptor 4metastasispeptideS100A8Toll‐like receptor 4tumor microenvironment

Identifiers

PMID39581861
PMCPMC11786323

What OpenQuestion holds

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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.