Evidence map›Paper›PMID 33468159›Full record

ArticleCancer cell international2021

IRF4 overexpression promotes the transdifferentiation of tregs into macrophage-like cells to inhibit the development of colon cancer.

Jiwei Wang, Song Li, Honglang Li, Xiaoshuang Zhou, Huabin Wen, Bin Lai

Abstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

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  10. Curcumin nanoparticles in heat stroke management.Journal of nanobiotechnology · 2024
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  18. Tumor Cell-Derived Exosomal miR-770 Inhibits M2 Macrophage PolarizationFrontiers in cell and developmental biology · 2021
    Article
  19. 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

6 authors.

Jiwei WangDepartment of Ultrasound, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.
Song LiMudanjiang Medical College, Mudanjiang, Heilongjiang, China.
Honglang LiDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, No 1. Minde Road, Nanchang, Jiangxi, 330006, China.
Xiaoshuang ZhouDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, No 1. Minde Road, Nanchang, Jiangxi, 330006, China.
Huabin WenDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, No 1. Minde Road, Nanchang, Jiangxi, 330006, China.
Bin LaiDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Nanchang University, No 1. Minde Road, Nanchang, Jiangxi, 330006, China. Vincent83126@163.com.ORCID http://orcid.org/0000-0001-8060-9980

Funding

National Natural Science Foundation of China 81960437Science and Technology Project of Jiangxi Province 20192BBGL70030Science and Technology Project of Jiangxi Province 20192BBH80025
6 · The paper itself

Abstract

backgroundInterferon regulatory factor 4 (IRF4) is a transcription factor from the IRF factor family that exerts regulatory functions in the immune system and oncogenesis. However, the biological role of IRF4 in colon cancer is still unclear. The aim of this study is to investigate whether IRF4 participates in the immune response in colon cancer.

methodsWe compared the expression of IRF4, the number of regulatory T cells (Tregs) and macrophages in the colon cancer tissues and paracancerous colon tissues from colon cancer patients. Colon cancer mouse model was established by inoculation with colon cancer cells (SW480) as a xenograft tumor, and we observed tumor growth of colon cancer. Furthermore, the mechanism of action of IRF4 in transdifferentiation of Tregs into macrophage-like cells and the effect of IRF4 on colon cancer cells were investigated in vitro.

resultsIRF4 was severely down-regulated in the colon cancer tissues. Colon cancer tissues exhibited an increase in the number of regulatory T cells (Tregs) and macrophages. Furthermore, IRF4 overexpression repressed proliferation, migration and invasion of colon cancer cells (SW480 and HT116 cells). Moreover, IRF4 up-regulation ameliorated tumor growth of colon cancer by promoting the transdifferentiation of Tregs into macrophage-like cells through inhibition of BCL6 expression. Exosomes derived from colon cancer cells repressed IRF4 expression in Tregs by transmitting miR-27a-3p, miR-30a-5p and miR-320c.

conclusionsIRF4 overexpression promoted the transdifferentiation of Tregs into macrophage-like cells to inhibit the occurrence and development of colon cancer. Thus, IRF4 may be a potential target for colon cancer treatment.

Indexed as

BCL6Colon cancerIRF4Macrophage‐like cellsmiRNAsTregs

Identifiers

PMID33468159
PMCPMC7816309

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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.