Evidence map›Paper›PMID 28106852›Full record

ArticleInternational journal of molecular sciences2017

Tumor-Derived Tissue Factor Aberrantly Activates Complement and Facilitates Lung Tumor Progression via Recruitment of Myeloid-Derived Suppressor Cells.

Xiao Han, Haoran Zha, Fei Yang, Bo Guo, Bo Zhu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  15. C5aR1 regulates migration of suppressive myeloid cells required for costimulatory blockade-induced murine allograft survival.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
    Article
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  17. Complementing the Cancer-Immunity Cycle.Frontiers in immunology · 2019
    Review
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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

5 authors at 2 institutions in 1 country.

Xiao HanInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China. hanx310@tmmu.edu.cn.
Haoran ZhaInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China. zhahaoran@tmmu.edu.cn.
Fei YangDepartment of Pathogenic Biology, Third Military Medical University, Chongqing 400037, China. yangf129@tmmu.edu.cn.
Bo GuoDepartment of Pathogenic Biology, Third Military Medical University, Chongqing 400037, China. guobo@tmmu.edu.cn.
Bo ZhuInstitute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China. bo.zhu@tmmu.edu.cn.
Army Medical University · CNXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The initiator of extrinsic coagulation, tissue factor (TF), and its non-coagulant isoform alternatively spliced TF (asTF) are closely associated with tumor development. In the tumor microenvironment, the role of TF-induced coagulation in tumor progression remains to be fully elucidated. Using TF-knockdown lung tumor cells, we showed that TF is the dominant component of procoagulant activity but is dispensable in the cellular biology of tumor cells. In a xenograft model, using immunohistochemical analysis and flow cytometry analysis of the tumor microenvironment, we demonstrated that TF-induced fibrin deposition, which is correlated with complement activation and myeloid-derived suppressor cell (MDSC) recruitment, is positively associated with tumor progression. C5aR antagonism blunted the effect of TF on tumor progression and decreased MDSC recruitment. In conclusion, our data suggested that in tumor microenvironment, TF-induced coagulation activated the complement system and subsequently recruited myeloid-derived suppressor cells to promote tumor growth, which brings new insights into the coagulation-induced complement activation within the tumor microenvironment during tumor progression.

Indexed as

Complement ActivationDisease ProgressionA549 CellsAnimalsApoptosisBlood CoagulationCell ProliferationFemaleGene Knockdown TechniquesHumansLung NeoplasmsMice, NudeMyeloid-Derived Suppressor CellsReceptor, Anaphylatoxin C5aThromboplastinReceptor, Anaphylatoxin C5aThromboplastincomplementmyeloid-derived suppressor cellstumor-derived tissue factor

Identifiers

PMID28106852
PMCPMC5297657
OpenAlexW2577040720

What OpenQuestion holds

Textmetadata
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.