Evidence map›Paper›PMID 27196773›Full record

ArticleMolecular cancer therapeutics2016

Emodin Inhibits Breast Cancer Growth by Blocking the Tumor-Promoting Feedforward Loop between Cancer Cells and Macrophages.

Stephen Iwanowycz, Junfeng Wang, Johnie Hodge, Yuzhen Wang, Fang Yu, Daping Fan

Abstract read
In one paragraph

Article in Molecular cancer therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
13.7field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 88 citations in OpenAlex.

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  16. Emodin reduces tumor burden by diminishing M2-like macrophages in colorectal cancer.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Article
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  20. Histone 3 Lysine 27 Trimethylation Signature in Breast Cancer.International journal of molecular sciences · 2021
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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

6 authors at 1 institution in 2 countries.

Stephen IwanowyczDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina.
Junfeng WangDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina.
Johnie HodgeDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina.
Yuzhen WangDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina.
Fang YuDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina. Department of Nutrition and Food Hygiene, Fourth Military Medical University, Xi'an, China.
Daping FanDepartment of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina. daping.fan@uscmed.sc.edu.
University of South Carolina · US

Funding

Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
Sparstolonin B as an anti-atherogenic agentR01HL116626 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FAN, DAPING · 2013 to 2017
$1.7M
NCCIH NIH HHS P01 AT003961NHLBI NIH HHS R01 HL116626
6 · The paper itself

Abstract

Macrophage infiltration correlates with severity in many types of cancer. Tumor cells recruit macrophages and educate them to adopt an M2-like phenotype through the secretion of chemokines and growth factors, such as MCP1 and CSF1. Macrophages in turn promote tumor growth through supporting angiogenesis, suppressing antitumor immunity, modulating extracellular matrix remodeling, and promoting tumor cell migration. Thus, tumor cells and macrophages interact to create a feedforward loop supporting tumor growth and metastasis. In this study, we tested the ability of emodin, a Chinese herb-derived compound, to inhibit breast cancer growth in mice and examined the underlying mechanisms. Emodin was used to treat mice bearing EO771 or 4T1 breast tumors. It was shown that emodin attenuated tumor growth by inhibiting macrophage infiltration and M2-like polarization, accompanied by increased T-cell activation and reduced angiogenesis in tumors. The tumor inhibitory effects of emodin were lost in tumor-bearing mice with macrophage depletion. Emodin inhibited IRF4, STAT6, and C/EBPβ signaling and increased inhibitory histone H3 lysine 27 tri-methylation (H3K27m3) on the promoters of M2-related genes in tumor-associated macrophages. In addition, emodin inhibited tumor cell secretion of MCP1 and CSF1, as well as expression of surface anchoring molecule Thy-1, thus suppressing macrophage migration toward and adhesion to tumor cells. These results suggest that emodin acts on both breast cancer cells and macrophages and effectively blocks the tumor-promoting feedforward loop between the two cell types, thereby inhibiting breast cancer growth and metastasis. Mol Cancer Ther; 15(8); 1931-42. ©2016 AACR.

Indexed as

AnimalsBiomarkersBreast NeoplasmsCell CommunicationCell Line, TumorCell SurvivalDisease Models, AnimalDose-Response Relationship, DrugEmodinFemaleGene Expression Regulation, NeoplasticHumansLymphocyte ActivationMacrophage ActivationMacrophagesMiceBiomarkersEmodinProtein Kinase Inhibitors

Identifiers

PMID27196773
PMCPMC4975665
OpenAlexW2404254617

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.