Evidence map›Paper›PMID 33558489›Full record

ArticleNature communications2021

Malignant subclone drives metastasis of genetically and phenotypically heterogenous cell clusters through fibrotic niche generation.

Sau Yee Kok, Hiroko Oshima, Kei Takahashi, Mizuho Nakayama, Kazuhiro Murakami, Hiroki R Ueda, Kohei Miyazono, Masanobu Oshima

Abstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Article
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  7. Mechanisms of metastatic colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. An In Vivo Metastasis Model Using Genotype-Defined Tumor Organoids.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  14. Cancer-Associated Fibroblast-Like Tumor Cells Remodel the Ewing Sarcoma Tumor Microenvironment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. Article
  16. Review
  17. Article
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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.

Sau Yee KokDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Hiroko OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Kei TakahashiDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Mizuho NakayamaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Kazuhiro MurakamiDivision of Epithelial Stem Cell Biology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
Hiroki R UedaDepartment of Systems Pharmacology, The University of Tokyo, Tokyo, Japan.
Kohei MiyazonoDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-7341-0172
Masanobu OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan. oshimam@staff.kanazawa-u.ac.jp.ORCID 0000-0002-3304-0004

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A concept of polyclonal metastasis has recently been proposed, wherein tumor cell clusters break off from the primary site and are disseminated. However, the involvement of driver mutations in such polyclonal mechanism is not fully understood. Here, we show that non-metastatic AP cells metastasize to the liver with metastatic AKTP cells after co-transplantation to the spleen. Furthermore, AKTP cell depletion after the development of metastases results in the continuous proliferation of the remaining AP cells, indicating a role of AKTP cells in the early step of polyclonal metastasis. Importantly, AKTP cells, but not AP cells, induce fibrotic niche generation when arrested in the sinusoid, and such fibrotic microenvironment promotes the colonization of AP cells. These results indicate that non-metastatic cells can metastasize via the polyclonal metastasis mechanism using the fibrotic niche induced by malignant cells. Thus, targeting the fibrotic niche is an effective strategy for halting polyclonal metastasis.

Indexed as

AnimalsCell AggregationCell ProliferationClone CellsFibrosisHepatic Stellate CellsLiverMiceMice, Inbred NODNeoplasm MetastasisNeoplasmsOrganoidsPhenotypeSpleenTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID33558489
PMCPMC7870854

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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.