Evidence map›Paper›PMID 35572560›Full record

ArticleFrontiers in immunology2022

Inhibition of CCCTC Binding Factor-Programmed Cell Death Ligand 1 Axis Suppresses Emergence of Chemoresistance Induced by Gastric Cancer-Derived Mesenchymal Stem Cells.

Qianqian Wang, Chao Huang, Ying Ding, Shaodi Wen, Xin Wang, Shuwei Guo, Qiuzhi Gao, Zhihong Chen, Yuanyuan Zhao, Mei Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Gastric cancer mesenchymal stem cells via the CXCR2/HK2/PD-L1 pathway mediate immunosuppression.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  8. 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

12 authors at 3 institutions in 1 country.

Qianqian WangSchool of Medicine, Jiangsu University, Zhenjiang, China.
Chao HuangSchool of Medicine, Jiangsu University, Zhenjiang, China.
Ying DingSchool of Medicine, Jiangsu University, Zhenjiang, China.
Shaodi WenDepartment of Oncology, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Xin WangDepartment of Oncology, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Shuwei GuoSchool of Medicine, Jiangsu University, Zhenjiang, China.
Qiuzhi GaoSchool of Medicine, Jiangsu University, Zhenjiang, China.
Zhihong ChenDepartment of Gastrointestinal Surgery, Affiliated People's Hospital of Jiangsu University, Zhenjiang, China.
Yuanyuan ZhaoSchool of Medicine, Jiangsu University, Zhenjiang, China.
Mei WangSchool of Medicine, Jiangsu University, Zhenjiang, China.
Bo ShenDepartment of Oncology, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Wei ZhuSchool of Medicine, Jiangsu University, Zhenjiang, China.
Jiangsu University · CNNanjing Medical University · CNJiangsu Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Gastric cancer (GC) is the third leading cause of cancer-associated deaths worldwide. Stromal cells, especially mesenchymal stem cells (MSCs), play significant roles in the development of therapy resistance depending on their paracrine function. The PD-1/PD-L1 crosstalk between cancer and immune cells has been well studied. Emerging evidence suggests that PD-L1 also contributes to tumor resistance to therapy. Methods: Cell survival and apoptosis were assessed using CCK-8, colony formation, and flow cytometry assays. Protein alterations were analyzed Results: In response to 5-fluorouracil or paclitaxel treatment, GCMSC-CM enhanced the cell viability and decreased the apoptosis rate. Furthermore, blocking PD-L1 or CTCF in GC cells prevented GCMSC-induced drug resistance accompanied by a decline in cell stemness. Consistent with these Conclusion: Study results demonstrate a mechanism where GCMSC-CM promotes GC chemoresistance by upregulating CTCF-PD-L1 and provide strong evidence in support of targeting CTCF-PD-L1 signaling as a strategy to prevent resistance in the clinic.

Indexed as

Mesenchymal Stem CellsStomach NeoplasmsAnimalsApoptosisB7-H1 AntigenCCCTC-Binding FactorDrug Resistance, NeoplasmFluorouracilHumansLigandsMiceMice, NudeB7-H1 AntigenCCCTC-Binding FactorFluorouracilLigands5-FUchemotherapy resistanceCTCFgastric cancermesenchymal stem cellspaclitaxelPD-L1

Identifiers

PMID35572560
PMCPMC9095388
OpenAlexW4224943624

What OpenQuestion holds

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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.