Evidence map›Paper›PMID 37421165›Full record

ArticleCancer science2023

CCL21-Ser expression in melanoma cells recruits CCR7

Megumi Miyamoto, Yuki Kawato, Ryonosuke Fujie, Kaoru Kurowarabe, Kakeru Fujiwara, Reika Nobusawa, Ryota Hayashi, Kei Iida, Izumi Ohigashi, Haruko Hayasaka

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. 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
0.5field-weighted citation impact, top 27% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  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

10 authors at 2 institutions in 1 country.

Megumi MiyamotoDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Yuki KawatoFaculty of Science and Engineering, Kindai University, Osaka, Japan.
Ryonosuke FujieDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Kaoru KurowarabeDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Kakeru FujiwaraDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Reika NobusawaDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Ryota HayashiDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Kei IidaDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.
Izumi OhigashiDivision of Experimental Immunology, Institute of Advanced Medical Sciences, University of Tokushima, Tokushima, Japan.
Haruko HayasakaDepartment of Science, Graduate School of Science and Engineering, Kindai University, Osaka, Japan.ORCID https://orcid.org/0000-0003-1694-9248
Kindai University · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCL21-Ser, a chemokine encoded by the Ccl21a gene, is constitutively expressed in the thymic epithelial cells and stromal cells of secondary lymphoid organs. It regulates immune cell migration and survival through its receptor CCR7. Herein, using CCL21-Ser-expressing melanoma cells and the Ccl21a-deficient mice, we demonstrated the functional role of cancer cell-derived CCL21-Ser in melanoma growth in vivo. The B16-F10 tumor growth was significantly decreased in Ccl21a-deficient mice compared with that in wild-type mice, indicating that host-derived CCL21-Ser contributes to melanoma proliferation in vivo. In Ccl21a-deficient mice, tumor growth of melanoma cells expressing CCL21-Ser was significantly enhanced, suggesting that CCL21-Ser from melanoma cells promotes tumor growth in the absence of host-derived CCL21-Ser. The increase in tumor growth was associated with an increase in the CCR7

Indexed as

MelanomaT-LymphocytesAnimalsChemokine CCL21MiceReceptors, CCR7Tumor MicroenvironmentChemokine CCL21Receptors, CCR7CCL21CCR7chemokinemelanomanaïve T cell

Identifiers

PMID37421165
PMCPMC10475776
OpenAlexW4383615400

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.