Evidence map›Paper›PMID 26800504›Full record

ArticleCancer science2016

ADAM23 is downregulated in side population and suppresses lung metastasis of lung carcinoma cells.

Masahide Ota, Satsuki Mochizuki, Masayuki Shimoda, Hitoshi Abe, Yuka Miyamae, Ken Ishii, Hiroshi Kimura, Yasunori Okada

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Integrins in cancer stem cells.Frontiers in cell and developmental biology · 2024
    Review
  3. Proteases Regulate Cancer Stem Cell Properties and Remodel Their Microenvironment.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
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  14. Article
  15. ADAMTS13: more than a regulator of thrombosis.International journal of hematology · 2016
    Review
  16. 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

8 authors at 3 institutions in 1 country.

Masahide OtaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Satsuki MochizukiDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Masayuki ShimodaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Hitoshi AbeDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Yuka MiyamaeDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Ken IshiiDepartment of Orthopedic Surgery, Keio University School of Medicine, Tokyo, Japan.
Hiroshi KimuraSecond Department of Internal Medicine and Respiratory Medicine, Nara Medical University, Kashihara, Japan.
Yasunori OkadaDepartment of Pathology, Keio University School of Medicine, Tokyo, Japan.
Keio University · JPNara Medical University · JPJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells contain a small population of cancer stem cells or cancer initiating cells, which can be enriched in the side population (SP) after fluorescence activated cell sorting. To examine the members of the ADAM, ADAMTS and MMP gene families related to phenotypes of the SP and the main population (MP), we screened the expression of all the members in the propagated SP and MP of A549 lung adenocarcinoma cells, and found that the relative expression ratio of ADAM23 in the MP to the SP is most highly increased, but none of them are increased in the SP. A similar result on the ADAM23 expression was obtained with another cell line, Calu-3 cells. Overexpression of ADAM23 inhibited colony formation, cell adhesion and migration, and knockdown of ADAM23 by shRNA showed the reverse effects. ADAM23-mediated suppression of colony formation, cell adhesion and migration was greatly reduced by treatment with neutralizing anti-ADAM23 antibody, anti-αvβ3 integrin antibody and/or ADAM23 disintegrin peptide. Expression of cancer stem cell-related genes, including AKRC1/2, TM4SF1 and NR0B1, was increased by knockdown of ADAM23. In addition, lung metastasis of A549 transfectants with different levels of ADAM23 expression was negatively regulated by the ADAM23 expression levels. Our data provide evidence that ADAM23 plays a role in suppression of cancer cell progression through interaction with αvβ3 integrin, and suggest that downregulation of ADAM23 in SP cells may contribute toward providing a cancer stem cell phenotype by facilitating the activity of integrin αvβ3.

Indexed as

ADAM ProteinsCarcinoma, Non-Small-Cell LungCell AdhesionCell Line, TumorGene Expression Regulation, NeoplasticHumansIntegrin alphaVbeta3Neoplasm MetastasisNeoplastic Stem CellsSide-Population CellsADAM23 protein, humanADAM ProteinsIntegrin alphaVbeta3ADAM23colony formationmetastasisnon-small cell lung carcinoma cellsside population

Identifiers

PMID26800504
PMCPMC4832861
OpenAlexW2337461693

What OpenQuestion holds

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Registered trials

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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.