Evidence map›Paper›PMID 26224317›Full record

ArticleMolecular biology of the cell2015

Tumor necrosis factor-related apoptosis-inducing ligand induces the expression of proinflammatory cytokines in macrophages and re-educates tumor-associated macrophages to an antitumor phenotype.

Jing Gao, Dongsheng Wang, Dan Liu, Min Liu, Yehua Ge, Minghong Jiang, Yanxin Liu, Dexian Zheng

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

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  16. Acetylation in Tumor Immune Evasion Regulation.Frontiers in pharmacology · 2021
    Review
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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

8 authors.

Jing GaoInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Dongsheng WangInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Dan LiuInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Min LiuInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Yehua GeInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Minghong JiangInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China jiangminghong@163.com liuyx2000@yeah.net.
Yanxin LiuInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Dexian ZhengInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences; and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising candidate for cancer therapy, because it can induce apoptosis in various tumor cells but not in most normal cells. Although it is well known that TRAIL and its receptors are expressed in many types of normal cells, including immune cells, their immunological effects and regulatory mechanisms are still obscure. In the present study, we demonstrated that TRAIL affected the activity of NF-κB (nuclear factor-κB) and the expression of its downstream proinflammatory cytokines IL-1β (interleukin-1β), IL-6, and tumor necrosis factor α in macrophages. TRAIL also induced microRNA-146a (miR-146a) expression in an NF-κB-dependent manner. As a result, miR-146a was involved as a negative-feedback regulator in the down-regulation of proinflammatory cytokine expression. In addition, the suppression of histone deacetylase (HDAC) activities by trichostatin A improved miR-146a expression due to the up-regulation of the DNA-binding activity of NF-κB at the miR-146a promoter in TRAIL-induced macrophages, suggesting that histone acetylation was involved in the suppression of miR-146a expression. Further investigation revealed that the HDAC subtype HDAC1 directly regulated the expression of miR-146a in TRAIL-stimulated macrophages. Finally, the TRAIL-sensitive human non small cell lung carcinoma cell line NCI-H460 was used to elucidate the physiological significance of TRAIL with respect to tumor-associated macrophages (TAMs). We demonstrated that TRAIL re-educated TAMs to an M1-like phenotype and induced cytotoxic effects in the tumor cells. These data provide new evidence for TRAIL in the immune regulation of macrophages and may shed light on TRAIL-based antitumor therapy in human patients.

Indexed as

AnimalsApoptosisCells, CulturedCytokinesDown-RegulationHistone DeacetylasesHumansInterleukin-1betaInterleukin-6Macrophages, PeritonealMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, NudeMicroRNAsCytokinesHistone DeacetylasesInterleukin-1betaInterleukin-6MicroRNAsMIRN146 microRNA, humanNF-kappa BTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor-alpha

Identifiers

PMID26224317
PMCPMC4569310

What OpenQuestion holds

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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.