Evidence map›Paper›PMID 31281466›Full record

ArticleJournal of Cancer2019

Exosomes from Macrophages Exposed to Apoptotic Breast Cancer Cells Promote Breast Cancer Proliferation and Metastasis.

Xiuyan Yu, Qun Zhang, Xuehui Zhang, Qing Han, Hui Li, Yiqing Mao, Xi Wang, Hongyan Guo, David M Irwin, Gang Niu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 44 citations in OpenAlex.

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  3. Response of MDA-MB231 cells to cisplatin and paclitaxel - viability, migration and gene expression estimation in mono- and co-culture with macrophages.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025
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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

11 authors at 3 institutions in 2 countries.

Xiuyan YuDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Qun ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Xuehui ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Qing HanDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Hui LiDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Yiqing MaoDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Xi WangDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Hongyan GuoDepartment of Gynaecology and Obstetrics, Peking University Third Hospital, Beijing 100191, China.
David M IrwinDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada.
Gang NiuBeijing N&N Genetech Company, Beijing 100082, China.
Huanran TanDepartment of Pharmacology, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191, China.
Peking University · CNUniversity of Toronto · CAAnnoroad Gene Technology (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes have recently become the subject of increasing research interest. Interactions between tumor and host cells via exosomes play crucial roles in the initiation, progression and invasiveness of breast cancer. In our study, we used exosomes isolated from a co-culture model of THP-1-derived macrophages exposed to apoptotic MCF-7 or MDA-MB-231 breast cancer cell line cells to investigate their effects on naïve MCF-7 or MDA-MB-231 cells in vitro and in vivo. This post-chemotherapy tumor microenvironment model allowed us to explore possible mechanisms that explain increased proliferation and metastasis of breast cancer seen in some patients. Our results suggest that while exosomes derived from macrophages normally inhibit proliferation and metastasis of MCF-7 or MDA-MB-231 cells, exposure of macrophages to breast cancer cells that have experienced chemotherapy are modified them to promote these processes. Exosomes from macrophages exposed to apoptotic cancer cells have increased amounts of IL-6 that increases the phosphorylation of STAT3, which likely explains the increased transcription of STAT3 target genes such as CyclinD1, MMP2 and MMP9. These observations suggest that the inhibition of exosome secretion and STAT3 signaling pathway activation might suppress the growth and metastasis of malignant tumors, and provide new targets for therapeutic treatment of malignant tumors after chemotherapy.

Indexed as

apoptosisbreast cancerexosomemetastasisSTAT3

Identifiers

PMID31281466
PMCPMC6590039
OpenAlexW2952644505

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.