Evidence map›Paper›PMID 28894087›Full record

ArticleNature communications2017

Hypoxia inducible factor HIF-1 promotes myeloid-derived suppressor cells accumulation through ENTPD2/CD39L1 in hepatocellular carcinoma.

David Kung-Chun Chiu, Aki Pui-Wah Tse, Iris Ming-Jing Xu, Jane Di Cui, Robin Kit-Ho Lai, Lynna Lan Li, Hui-Yu Koh, Felice Ho-Ching Tsang, Larry Lai Wei, Chun-Ming Wong and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 276 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
276citing papers in PubMed, 1 pooled it
12.9field-weighted citation impact, top 1% 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

276 citing papers in PubMed, 1 synthesis or guideline pooled it, 447 citations in OpenAlex.

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  10. CD39Science translational medicine · 2026
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216 more citing papers are in PubMed but not listed here.

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

12 authors at 1 institution in 1 country.

David Kung-Chun ChiuDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Aki Pui-Wah TseDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Iris Ming-Jing XuDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Jane Di CuiDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Robin Kit-Ho LaiDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Lynna Lan LiDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Hui-Yu KohDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Felice Ho-Ching TsangDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Larry Lai WeiDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.
Chun-Ming WongDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong.ORCID http://orcid.org/0000-0002-2497-7858
Irene Oi-Lin NgDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong. iolng@hku.hk.
Carmen Chak-Lui WongDepartment of Pathology, The University of Hong Kong, Hong Kong, Hong Kong. carmencl@pathology.hku.hk.
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) possess immunosuppressive activities, which allow cancers to escape immune surveillance and become non-responsive to immune checkpoints blockade. Here we report hypoxia as a cause of MDSC accumulation. Using hepatocellular carcinoma (HCC) as a cancer model, we show that hypoxia, through stabilization of hypoxia-inducible factor-1 (HIF-1), induces ectoenzyme, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2/CD39L1), in cancer cells, causing its overexpression in HCC clinical specimens. Overexpression of ENTPD2 is found as a poor prognostic indicator for HCC. Mechanistically, we demonstrate that ENTPD2 converts extracellular ATP to 5'-AMP, which prevents the differentiation of MDSCs and therefore promotes the maintenance of MDSCs. We further find that ENTPD2 inhibition is able to mitigate cancer growth and enhance the efficiency and efficacy of immune checkpoint inhibitors. Our data suggest that ENTPD2 may be a good prognostic marker and therapeutic target for cancer patients, especially those receiving immune therapy.Myeloid-derived suppressor cells (MDSCs) promote tumor immune escape. Here, the authors show that in hepatocellular carcinoma, hypoxia induces the expression of ENTPD2 on cancer cells leading to elevated extracellular 5'-AMP, which in turn promote the maintenance of MDSCs by preventing their differentiation.

Indexed as

Adenosine TriphosphatasesCarcinoma, HepatocellularCell DifferentiationCell ProliferationHumansHypoxiaHypoxia-Inducible Factor 1Liver NeoplasmsMyeloid-Derived Suppressor CellsAdenosine TriphosphatasesectoATPaseHypoxia-Inducible Factor 1

Identifiers

PMID28894087
PMCPMC5593860
OpenAlexW2753173755

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.