Evidence map›Paper›PMID 26016502›Full record

ArticleInternational journal of molecular sciences2015

Exposure of tumor-associated macrophages to apoptotic MCF-7 cells promotes breast cancer growth and metastasis.

Na Zhou, Yizhuang Zhang, Xuehui Zhang, Zhen Lei, Ruobi Hu, Hui Li, Yiqing Mao, Xi Wang, David M Irwin, Gang Niu and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 43 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

11 authors at 1 institution in 2 countries.

Na ZhouDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. zhouna@bjmu.edu.cn.
Yizhuang ZhangDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. onepiecezyz1989@gmail.com.
Xuehui ZhangDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. xuehuizhang@bjmu.edu.cn.
Zhen LeiBeijing N&N Genetech Company, Beijing 100082, China. tanlab232@gmail.com.
Ruobi HuDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. huruobi@bjmu.edu.cn.
Hui LiDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. lihui@bjmu.edu.cn.
Yiqing MaoDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. maoyiqing@bjmu.edu.cn.
Xi WangDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. xixi1125@bjmu.edu.cn.
David M IrwinDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. david.irwin@utoronto.ca.
Gang NiuBeijing N&N Genetech Company, Beijing 100082, China. 59023@bjmu.edu.cn.
Huanran TanDepartment of Pharmacology, Peking University, Health Science Center, Beijing 100191, China. tanlab@bjmu.edu.cn.
Peking University · CN

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) have been found to be associated with the progression and metastasis of breast cancer. To clarify the mechanisms underlying the crosstalk between TAMs and cancer stem cells (CSCs) in breast cancer recurrence and metastasis, we used a co-culture model of macrophages and apoptotic human breast cancer cell line MCF-7 cells to investigate the effects of TAMs on MCF-7 in vitro and in vivo. Macrophages co-cultured with apoptotic MCF-7 had increased tumor growth and metastatic ability in a nude mouse transplantation assay. The macrophages exposed to apoptotic cells also induce an increase in the proportion of CD44+/CD24- cancer stem-like cells, as well as their proliferative ability accompanied with an increase in mucin1 (MUC1) expression. During this process, macrophages secreted increased amounts of interleukin 6 (IL-6) leading to increased phosphorylation of signal transducers and activators of transcription 3 (STAT3), which likely explains the increased transcription of STAT3 target genes such as TGF-β1 and HIF-1α. Our results indicate that when cancer cells endure chemotherapy induced apoptosis, macrophages in their microenvironment can then activate cancer stem cells to promote cancer growth and metastasis by secreting IL-6, which activates STAT3 phosphorylation to regulate the transcription of its downstream target genes.

Indexed as

AnimalsBreast NeoplasmsCell MovementCell ProliferationCells, CulturedCoculture TechniquesFemaleHumansInterleukin-6MacrophagesMCF-7 CellsMiceMice, NudeMucin-1Neoplasm MetastasisNeoplasm TransplantationInterleukin-6muc1 protein, mouseMucin-1Stat3 protein, mouseSTAT3 Transcription Factorapoptosiscancer stem cellsIL-6metastasisSTAT3TAMs

Identifiers

PMID26016502
PMCPMC4490423
OpenAlexW1534965343

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.