Evidence map›Paper›PMID 32564199›Full record

ArticleHuman cell2020

CCL19 suppresses gastric cancer cell proliferation, migration, and invasion through the CCL19/CCR7/AIM2 pathway.

Rui Zhou, Jun Sun, Chunping He, Chao Huang, Honggang Yu

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Natural and Engineered Cytokines as Cancer Therapeutics.Annual review of cancer biology · 2026
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  11. Review
  12. Article
  13. Article
  14. Article
  15. No Time to Die: How Kidney Cancer Evades Cell Death.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Does CCL19 act as a double-edged sword in cancer development?Clinical and experimental immunology · 2022
    Review
  18. Article
  19. Review
  20. 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

5 authors at 2 institutions in 1 country.

Rui ZhouDepartment of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhangzhidong Road, Wuhan, 430060, Hubei, People's Republic of China.
Jun SunDepartment of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhangzhidong Road, Wuhan, 430060, Hubei, People's Republic of China.
Chunping HeDepartment of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhangzhidong Road, Wuhan, 430060, Hubei, People's Republic of China.
Chao HuangDepartment of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhangzhidong Road, Wuhan, 430060, Hubei, People's Republic of China.
Honggang YuDepartment of Gastroenterology, Renmin Hospital of Wuhan University, No. 99 Zhangzhidong Road, Wuhan, 430060, Hubei, People's Republic of China. doctoryuhg@163.com.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Absent in melanoma 2 (AIM2) has been reported to be an important inflammasome component that exerts tumor suppression in several tumors. However, whether CCL19/CCR7/AIM2 is involved in the progression of GC still remains unclear. Quantitative real-time and ELISA assay were used to determine the expressions of AIM2, CCL19 and CCR7 in GC tissues and cell lines. CCK-8, Edu staining, flow cytometry, Transwell assay, and tumorigenesis in nude mice were used to explore the function of AIM2 and CCL19 in vitro and in vivo. Apoptosis and inflammation-related biomarkers were detected by Western blot and ELISA assay. H&E staining was used to assess the histological changes in the subcutaneous tumor model. Immunohistochemistry (IHC) was used to evaluate the expression of Ki-67. We found that expression levels of AIM2, CCL19 and CCR7 were obviously lower in early GC tissues than those in progressive GC tissues. In vitro assays revealed that CCL19 treatment could enhance the suppressive effects of AIM2 overexpression on cell proliferation, migration, and invasion through CCR7. An in vivo assay also demonstrated that silencing of AIM2 reversed the suppressive effects of CCL19 on tumor growth. Collectively, CCL19 overexpression significantly inhibited GC cell proliferation and tumor growth in vitro and in vivo by up-regulating the CCR7/AIM2 pathway. Thus, CCL19 activated CCR7/AIM2 signaling pathway and it may be a potential therapeutic approach for GC therapy.

Indexed as

Cell Line, TumorCell MovementCell ProliferationChemokine CCL19Disease ProgressionDNA-Binding ProteinsGene ExpressionHumansMolecular Targeted TherapyNeoplasm InvasivenessReceptors, CCR7Signal TransductionStomach NeoplasmsAIM2 protein, humanCCL19 protein, humanCCR7 protein, humanChemokine CCL19DNA-Binding ProteinsReceptors, CCR7AIM2CCL19/CCR7Gastric cancerInflammationTumor growth

Identifiers

PMID32564199
OpenAlexW3035865799

What OpenQuestion holds

Textmetadata
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.