Evidence map›Paper›PMID 38625488›Full record

ArticleIn vitro cellular & developmental biology. Animal2024

Tumor endothelial cell-derived Sfrp1 supports the maintenance of cancer stem cells via Wnt signaling.

Yumiko Hayashi, Masakazu Hashimoto, Katsuyoshi Takaoka, Tatsuya Takemoto, Nobuyuki Takakura, Hiroyasu Kidoya

Open access · hybridAbstract read
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. 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

6 authors at 3 institutions in 1 country.

Yumiko HayashiDepartment of Integrative Vascular Biology, Faculty of Medical Science, Fukui University, 23-3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan.
Masakazu HashimotoLaboratory for Embryogenesis, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka, Japan.
Katsuyoshi TakaokaLaboratory for Embryology, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.
Tatsuya TakemotoLaboratory for Embryology, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.
Nobuyuki TakakuraDepartment of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Hiroyasu KidoyaDepartment of Integrative Vascular Biology, Faculty of Medical Science, Fukui University, 23-3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, 910-1193, Japan. kidoya@u-fukui.ac.jp.ORCID http://orcid.org/0000-0003-0413-7816
The University of Osaka · JPTokushima University · JPUniversity of Fukui · JP

Funding

Fusion Oriented REsearch for disruptive Science and Technology JPMJFR2160Japan Society for the Promotion of Science 19H03503Japan Society for the Promotion of Science 23H03860Japan Society for the Promotion of Science 23H03862Precursory Research for Embryonic Science and Technology JPMJPR1944
6 · The paper itself

Abstract

Cancer stem cells (CSCs), which are critical targets for cancer therapy as they are involved in drug resistance to anticancer drugs, and metastasis, are maintained by angiocrine factors produced by particular niches that form within tumor tissue. Secreted frizzled-related protein 1 (Sfrp1) is an extracellular protein that modulates Wnt signaling. However, the cells that produce Sfrp1 in the tumor environment and its function remain unclear. We aimed to elucidate angiocrine factors related to CSC maintenance, focusing on Sfrp1. Although Sfrp1 is a Wnt pathway-related factor, its impact on tumor tissues remains unknown. We investigated the localization of Sfrp1 in tumors and found that it is expressed in some tumor vessels. Analysis of mice lacking Sfrp1 showed that tumor growth was suppressed in Sfrp1-deficient tumor tissues. Flow cytometry analysis indicated that CSCs were maintained in the early tumor growth phase in the Sfrp1 knockout (KO) mouse model of tumor-bearing cancer. However, tumor growth was inhibited in the late tumor growth phase because of the inability to maintain CSCs. Real-time PCR results from tumors of Sfrp1 KO mice showed that the expression of Wnt signaling target genes significantly decreased in the late stage of tumor growth. This suggests that Sfrp1, an angiocrine factor produced by the tumor vascular niche, is involved in Wnt signaling-mediated mechanisms in tumor tissues.

Indexed as

Intercellular Signaling Peptides and ProteinsMembrane ProteinsMice, KnockoutNeoplastic Stem CellsWnt Signaling PathwayAnimalsCell Line, TumorEndothelial CellsHumansMiceSecreted Frizzled-Related ProteinsIntercellular Signaling Peptides and ProteinsMembrane ProteinsSecreted Frizzled-Related ProteinsSfrp1 protein, mouseAngiocrine factorCancer stem cellSfrp1Tumor endothelial cellWnt signaling

Identifiers

PMID38625488
PMCPMC11655579
OpenAlexW4394853325

What OpenQuestion holds

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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.