Evidence map›Paper›PMID 31769216›Full record

ArticleCancer medicine2020

p65/miR-23a/CCL22 axis regulated regulatory T cells recruitment in hepatitis B virus positive hepatocellular carcinoma.

Zhi-Qin Li, Hong-Yan Wang, Qing-Lei Zeng, Jing-Ya Yan, Yu-Shu Hu, Hua Li, Zu-Jiang Yu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. 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

7 authors at 1 institution in 1 country.

Zhi-Qin LiDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Hong-Yan WangDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Qing-Lei ZengDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Jing-Ya YanDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Yu-Shu HuDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Hua LiDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Zu-Jiang YuDepartment of Infectious Disease, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.ORCID 0000-0002-2096-2173
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCCL22 played critical roles in Tregs recruitment. The upstream regulators modulating CCL22 in hepatocellular carcinoma (HCC) were not clearly understood.

methodsMiR-23a, p-p65, p65, CCL22, and Foxp3 levels were monitored by RT-qPCR and western blotting. Immunofluorescence assay was used to perform the costaining of Foxp3 and CD4 on liver tissues. Transwell assay was applied to evaluate the migration ability of Tregs. Dual-luciferase assay was performed to determine relationship of miR-23a/CCL22 and p65/miR-23a. Chromatin immunoprecipitation (ChIP) was applied to detect the direct binding of p65 to miR-23a promoter. Xenograft tumor models were developed to investigate the functions of p65 and miR-23a in vivo.

resultsHBV infection was associated with reduced survival and increased Tregs recruitment in HCC patients. MiR-23a was decreased, whereas p65, CCL22, and Foxp3 were increased in HBV

conclusionBlockage of p65 disinhibited miR-23a expression, leading to CCL22 reduction and repress Tregs recruitment. Targeting p65/miR-23a/CCL22 axis was a novel approach for HBV

Indexed as

AnimalsApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell ProliferationChemokine CCL22FemaleGene Expression Regulation, NeoplasticHepatitis BHepatitis B virusHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeBiomarkers, TumorCCL22 protein, humanChemokine CCL22MicroRNAsMIRN23a microRNA, humanTranscription Factor RelACCL22HBVhepatocellular carcinomaMiR-23ap65Tregs recruitment

Identifiers

PMID31769216
PMCPMC6970059
OpenAlexW2989827657

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.