Evidence map›Paper›PMID 31663424›Full record

ArticleCancer biology & therapy2020

Antitumor properties of triptolide: phenotype regulation of macrophage differentiation.

Han Li, Liping Li, Huifang Mei, Guofeng Pan, Xinzhi Wang, Xin Huang, Tao Wang, Zhenzhou Jiang, Luyong Zhang, Lixin Sun

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Han LiJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Liping LiJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Huifang MeiJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Guofeng PanDepartment of TCM, Beijing Shijitan Hospital Affiliated with Capital Medical University, Beijing, China.
Xinzhi WangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Xin HuangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Tao WangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Zhenzhou JiangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Luyong ZhangJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
Lixin SunJiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, China.
China Pharmaceutical University · CNBeijing Shijitan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs), which generally exhibit an M2-like phenotype, play a critical role in tumor development. Triptolide exerts a unique bioactive spectrum of anticancer activities. The aim of this study was to determine whether triptolide has any effect on the activation of TAMs and the production of tumor-promoting mediators. ICR-1 mice with azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colon tumors and BALB/c mice co-inoculated with 4T1 cells and M2-polarized RAW264.7 cells were used to examine whether the inhibitory effect of triptolide on tumor progression was mediated by the targeting of TAMs. Real-time PCR, Western blot, immunofluorescence staining, and flow cytometry assays were performed to determine the expression of cell surface markers and cytokine production. The results showed that triptolide inhibited macrophage differentiation toward the M2 phenotype and abolished M2 macrophage-mediated tumor progression. Furthermore, triptolide inhibited the expression of M2 markers, such as CD206, Arginase 1, and CD204, and inhibited the secretion of anti-inflammatory cytokines. Thus our study indicated that triptolide selectively inhibited the functions of M2-polarized macrophages and TAMs, and this inhibitory effect of triptolide on TAM viability, differentiation, and cytokine production might elucidate the major mechanisms underlying its antitumor activity. Our findings provide important information for the potential clinical application of triptolide in cancer therapy.

Indexed as

Tumor MicroenvironmentAnimalsAntineoplastic Agents, AlkylatingApoptosisBreast NeoplasmsCell DifferentiationCell ProliferationColonic NeoplasmsDiterpenesEpoxy CompoundsFemaleHumansMiceMice, Inbred BALB CMice, Inbred ICRMice, NudeAntineoplastic Agents, AlkylatingDiterpenesEpoxy CompoundsPhenanthrenestriptolidebreast cancercolitis-associated colon cancerM2-polarizedtriptolideTumor-associated macrophagestumor growth

Identifiers

PMID31663424
PMCPMC7012063
OpenAlexW2982689046

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.