Evidence map›Paper›PMID 27375023›Full record

ArticleOncogene2017

TNFα-activated mesenchymal stromal cells promote breast cancer metastasis by recruiting CXCR2

P F Yu, Y Huang, Y Y Han, L Y Lin, W H Sun, A B Rabson, Y Wang, Y F Shi

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 3 pooled it
12.9field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 3 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Pooled it
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  7. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
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87 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

P F YuKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
Y HuangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0001-5602-9871
Y Y HanKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
L Y LinKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
W H SunKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
A B RabsonChild Health Institute of New Jersey, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Y WangKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
Y F ShiKey Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences/Shanghai Jiao Tong University School of Medicine, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
Shanghai Jiao Tong University · CNRutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stromal cells (MSCs) tend to infiltrate into tumors and form a major component of the tumor microenvironment. Our previous work demonstrated that tumor necrosis factor α (TNFα)-activated MSCs significantly promoted tumor growth. However, the role of TNFα-treated MSCs in tumor metastasis remains elusive. Employing a lung metastasis model of murine breast cancer, we found that TNFα-activated MSCs strikingly enhanced tumor metastasis compared with normal MSCs. We analyzed the chemokine profiles and found that the expression of CCL5, CCR2 and CXCR2 ligands were enhanced in TNFα-activated MSCs. Using genetic or pharmacological strategies to inhibit CCL5 or CCR2, we demonstrated that CCL5 and CCR2 ligands were indispensable in supporting TNFα-activated MSCs to promote tumor metastasis. Analysis of immune cells revealed that CXCR2 ligands (CXCL1, CXCL 2 and CXCL5) expressed by TNFα-activated MSCs efficiently recruited CXCR2

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorFemaleHumansLung NeoplasmsMesenchymal Stem CellsMiceMice, Inbred BALB CNeoplasm MetastasisNeutrophilsReceptors, Interleukin-8BSignal TransductionTumor Necrosis Factor-alphaReceptors, Interleukin-8BTumor Necrosis Factor-alpha

Identifiers

PMID27375023
PMCPMC5290040
OpenAlexW2460847595

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.