Evidence map›Paper›PMID 35102665›Full record

ArticleCancer science2022

Serum amyloid A 1 induces suppressive neutrophils through the Toll-like receptor 2-mediated signaling pathway to promote progression of breast cancer.

Xingjian Niu, Lei Yin, Xudong Yang, Yue Yang, Yucui Gu, Yutian Sun, Ming Yang, Yiran Wang, Qingyuan Zhang, Hongfei Ji

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  9. HAX1 inhibits apoptosis and promotes maturation of neutrophils.Cell communication and signaling : CCS · 2025
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  11. Article
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  13. Review
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  19. p53 deficient breast cancer cells reprogram preadipocytes toward tumor-protective immunomodulatory cells.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article
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

10 authors at 1 institution in 1 country.

Xingjian NiuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, China.
Lei YinInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, China.
Xudong YangInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, China.
Yue YangInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, China.
Yucui GuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, China.
Yutian SunDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, China.
Ming YangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, China.
Yiran WangInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, China.
Qingyuan ZhangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, China.ORCID https://orcid.org/0000-0001-7618-4393
Hongfei JiInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, China.ORCID https://orcid.org/0000-0002-1452-1697
Harbin Medical University · CN

Funding

China Postdoctoral Science Foundation 2018M641858National Natural Science Foundation of China 82002781Postdoctoral Foundation of Hei Long Jiang Province LBH-Z18115the Science and Technology Foundation of Finance Bureau of Heilongjiang Province CZKYF2021B004
6 · The paper itself

Abstract

Immune inflammation plays a key role in breast cancer development, progression, and therapeutic efficacy. Neutrophils are crucial for the regulation of the suppressive tumor microenvironment and are associated with poor clinical survival. However, the mechanisms underlying the activation of suppressive neutrophils in breast cancer are poorly understood. Here, we report that breast cancer cells secrete abundant serum amyloid A 1 (SAA1), which is associated with the accumulation of suppressive neutrophils. High expression of SAA1 in breast cancer induces neutrophil immunosuppressive cytokine production through the activation of Toll-like receptor 2 (TLR2)-mediated signaling pathways. These include the TLR2/myeloid differentiation primary response 88 (MYD88)-mediated PI3K/nuclear factor-κB signaling pathway and p38 MAPK-associated apoptosis resistance pathway, which eventually promote the progression of breast cancer. Our study shows a mechanistic link between breast cancer cell secretion of SAA1 and suppressive neutrophils that potentiate tumor progression. These findings provide potential therapeutic targets for breast cancer.

Indexed as

Breast NeoplasmsSerum Amyloid A ProteinFemaleHumansNeutrophilsNF-kappa BSignal TransductionToll-Like Receptor 2Tumor MicroenvironmentNF-kappa BSerum Amyloid A ProteinToll-Like Receptor 2breast cancerneutrophilserum amyloid AsuppressiveTLR2

Identifiers

PMID35102665
PMCPMC8990718
OpenAlexW4210577518

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.