Evidence map›Paper›PMID 33565179›Full record

ArticleCancer science2021

ASK1 suppresses NK cell-mediated intravascular tumor cell clearance in lung metastasis.

Makoto Fujimoto, Miki Kamiyama, Kosuke Fuse, Hiroki Ryuno, Takeru Odawara, Natsuki Furukawa, Yasuhiro Yoshimatsu, Tetsuro Watabe, Michaela Prchal-Murphy, Veronika Sexl and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2021. 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
0.5field-weighted citation impact, top 41% 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, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. 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

16 authors at 7 institutions in 2 countries.

Makoto FujimotoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-8151-4913
Miki KamiyamaLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-9817-6703
Kosuke FuseLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Hiroki RyunoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Takeru OdawaraLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Natsuki FurukawaLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Yasuhiro YoshimatsuDivision of Pharmacology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Tetsuro WatabeDepartment of Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.ORCID https://orcid.org/0000-0001-5836-1309
Michaela Prchal-MurphyDepartment of Biomedical Sciences, Institute of Pharmacology and Toxicology, University of Veterinary Medicine of Vienna, Wien, Austria.
Veronika SexlDepartment of Biomedical Sciences, Institute of Pharmacology and Toxicology, University of Veterinary Medicine of Vienna, Wien, Austria.
Hideaki TaharaDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, Osaka, Japan.ORCID https://orcid.org/0000-0002-1735-5372
Yoshihiro HayakawaDivision of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama, Japan.ORCID https://orcid.org/0000-0002-7921-1171
Takehiro SatoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Kohsuke TakedaDivision of Cell Regulation, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.ORCID https://orcid.org/0000-0002-8359-8399
Isao NaguroLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Hidenori IchijoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-5005-6438
The University of Tokyo · JPUniversity of Veterinary Medicine Vienna · ATNagasaki University · JPNiigata University · JPThe Cancer Institute Hospital · JPTokyo Medical and Dental University · JPUniversity of Toyama · JP

Funding

Japan Agency for Medical Research and Development JP20gm5010001Japan Science and Technology Agency JPMJMS2022-18Japan Society for the Promotion of Science 18K19469Japan Society for the Promotion of Science JP15K14445Japan Society for the Promotion of Science JP17H06419Japan Society for the Promotion of Science JP18H02569Japan Society for the Promotion of Science JP18H03995Japan Society for the Promotion of Science JP18K19469Japan Society for the Promotion of Science JP26114009Yasuda Memorial Medical Foundation 2017Y-1
6 · The paper itself

Abstract

Tumor metastasis is the leading cause of death worldwide and involves an extremely complex process composed of multiple steps. Our previous study demonstrated that apoptosis signal-regulating kinase 1 (ASK1) deficiency in mice attenuates tumor metastasis in an experimental lung metastasis model. However, the steps of tumor metastasis regulated by ASK1 remain unclear. Here, we showed that ASK1 deficiency in mice promotes natural killer (NK) cell-mediated intravascular tumor cell clearance in the initial hours of metastasis. In response to tumor inoculation, ASK1 deficiency upregulated immune response-related genes, including interferon-gamma (IFNγ). We also revealed that NK cells are required for these anti-metastatic phenotypes. ASK1 deficiency augmented cytokine production chemoattractive to NK cells possibly through induction of the ligand for NKG2D, a key activating receptor of NK cells, leading to further recruitment of NK cells into the lung. These results indicate that ASK1 negatively regulates NK cell-dependent anti-tumor immunity and that ASK1-targeted therapy can provide a new tool for cancer immunotherapy to overcome tumor metastasis.

Indexed as

AnimalsCell LineCell Line, TumorFemaleHEK293 CellsHumansImmunotherapyInterferon-gammaKiller Cells, NaturalLungLung NeoplasmsMAP Kinase Kinase Kinase 5MiceMice, Inbred C57BLNeoplasm MetastasisRAW 264.7 CellsInterferon-gammaMap3k5 protein, mouseMAP Kinase Kinase Kinase 5ASK1intravascular tumor cell clearancelung metastasisNK cellNKG2D

Identifiers

PMID33565179
PMCPMC8019214
OpenAlexW3127089713

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.