Evidence map›Paper›PMID 34306099›Full record

ArticleStem cells international2021

Gastric Cancer Mesenchymal Stem Cells Inhibit NK Cell Function through mTOR Signalling to Promote Tumour Growth.

Shuwei Guo, Chao Huang, Fengfeng Han, Bin Chen, Ying Ding, Yuanyuan Zhao, Zhihong Chen, Shaodi Wen, Mei Wang, Bo Shen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cells international, 2021. 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
2.0field-weighted citation impact, top 13% 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, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Immunology and immunotherapy in gastric cancer.Clinical and experimental medicine · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Mesenchymal Stem Cell: A Friend or Foe in Anti-Tumor Immunity.International journal of molecular sciences · 2021
    Review
  15. 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

11 authors at 2 institutions in 1 country.

Shuwei GuoSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Chao HuangSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Fengfeng HanSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Bin ChenSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Ying DingSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Yuanyuan ZhaoSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Zhihong ChenDepartment of Gastrointestinal Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
Shaodi WenDepartment of Oncology, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu, China.
Mei WangSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Bo ShenDepartment of Oncology, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu, China.
Wei ZhuSchool of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.ORCID https://orcid.org/0000-0002-5237-1992
Jiangsu University · CNJiangsu Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dysfunction of natural killer (NK) cells has been increasingly reported in malignancies, especially in solid tumours. Mesenchymal stem cells (MSCs) exhibit pleiotropic functions that include mediating immune cell exhaustion which is implicated in cancer progression. However, the association of MSCs derived from gastric cancer (gastric cancer mesenchymal stem cells: GCMSCs) with the dysfunction of NK cells remains poorly understood. In this study, we demonstrated that GCMSCs effectively contributed to the exhaustion of NK cells through the release of soluble factors. Furthermore, passivation of the antitumour effect in NK cells was closely associated with their dysfunctional state. The GCMSC-conditioned medium prevented the frequency and effector function of infiltrating NK cells in tumour-bearing mouse models, thus promoting tumour growth. Mechanistically, mammalian target of rapamycin (mTOR) signalling, a critical regulator of cellular metabolism that mediates the function of immune cells, was inhibited in NK cells treated with GCMSCs. However, the checkpoint receptor PD-1 was still present at minimal levels with or without GCMSCs. The study results revealed that GCMSCs contributed to dysfunctional NK cells involved at least partially in the inhibition of mTOR signalling, suggesting potential directions for NK cell-based cancer immunotherapy.

Identifiers

PMID34306099
PMCPMC8263240
OpenAlexW3173782511

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.