Evidence map›Paper›PMID 36359867›Full record

ArticleCells2022

Curcumin Reprograms TAMs from a Protumor Phenotype towards an Antitumor Phenotype via Inhibiting MAO-A/STAT6 Pathway.

Mingjing Jiang, Ying Qi, Wei Huang, Ying Lin, Bo Li

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  15. Effects of macrophages in OSCC progression.Frontiers in immunology · 2024
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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.

Mingjing JiangLiaoning Provincial Key Laboratory of Oral Diseases, Experimental Teaching Center, School and Hospital of Stomatology, China Medical University, Shenyang 110001, China.ORCID 0000-0003-2873-1924
Ying QiLiaoning Provincial Key Laboratory of Oral Diseases, Experimental Teaching Center, School and Hospital of Stomatology, China Medical University, Shenyang 110001, China.ORCID 0000-0002-9694-393X
Wei HuangLiaoning Provincial Key Laboratory of Oral Diseases, Experimental Teaching Center, School and Hospital of Stomatology, China Medical University, Shenyang 110001, China.ORCID 0000-0002-0665-9768
Ying LinLiaoning Provincial Key Laboratory of Oral Diseases, Experimental Teaching Center, School and Hospital of Stomatology, China Medical University, Shenyang 110001, China.ORCID 0000-0003-0560-9424
Bo LiLiaoning Provincial Key Laboratory of Oral Diseases, Experimental Teaching Center, School and Hospital of Stomatology, China Medical University, Shenyang 110001, China.ORCID 0000-0002-6005-6351
China Medical University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

M1 phenotype macrophages have anticancer characteristics, whereas M2 phenotype macrophages promote tumor growth and metastasis. A higher M1/M2 ratio, therefore, has a beneficial effect on the tumor immune microenvironment, thereby inhibiting tumor growth. The natural alkaloid curcumin is found to have anticancer properties. However, the mechanism remains unclear. In this study, a cell co-culture system and M2 macrophage model were used to evaluate the effects of curcumin on tumor-associated macrophage (TAM) phenotypes. Our results demonstrate that curcumin reprogrammed the M2 macrophages by reducing the level of anti-inflammatory cytokines (TGF-β, Arg-1, and IL-10) and an M2 surface marker (CD206) induced by Cal27 cells or IL-4, as well as upregulating proinflammatory cytokines (TNF-α, iNOS, and IL-6) and an M1 surface marker (CD86). The in vitro assays suggested that curcumin treatment suppressed the migration and invasion of the Cal27 cells induced by the M2-like macrophages. Mechanistically, the repolarization of TAMs may be attributed to the inhibition of monoamine oxidase A (MAO-A)/STAT6 signaling after curcumin treatment. Collectively, our results show that the anticancer effects of curcumin could be explained by reprogramming TAMs from a protumor phenotype towards an antitumor phenotype.

Indexed as

CurcuminCytokinesMacrophagesMonoamine OxidasePhenotypeCurcuminCytokinesMonoamine Oxidasecurcuminimmunotherapyrepolarization

Identifiers

PMID36359867
PMCPMC9655729
OpenAlexW4309091296

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.