Evidence map›Paper›PMID 32669478›Full record

ArticleAging2020

C5aR deficiency attenuates the breast cancer development via the p38/p21 axis.

Jian Chen, Zi-Han Sun, Li-Ying Chen, Feng Xu, Yun-Pei Zhao, Gui-Qing Li, Ming Tang, You Li, Quan-You Zheng, Shu-Feng Wang and 3 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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  12. C5aR1 promotes the progression of colorectal cancer by EMT and activating Wnt/β-catenin pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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

13 authors at 3 institutions in 1 country.

Jian ChenDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Zi-Han SunBreast Disease Center, Guiqian International General Hospital, Guiyang 550000, China.
Li-Ying ChenInstitute of Cancer, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing 400037, China.
Feng XuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Yun-Pei ZhaoDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Gui-Qing LiDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Ming TangUrinary Nephropathy Center, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400065, China.
You LiDepartment of ICU, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Quan-You ZhengDepartment of Urology, 958 Hospital, Army Medical University (Third Military Medical University), Chongqing 400020, China.
Shu-Feng WangDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Xin-Hua YangBreast Disease Center, Guiqian International General Hospital, Guiyang 550000, China.
Yu-Zhang WuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Gui-Lian XuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Army Medical University · CNDalian Medical University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence has shown activation of the complement component C5 to C5a in cancer tissues and C5aR expression in breast cancer cells relates to the tumor development and poor prognosis, suggesting the involvement of complement C5a/C5aR pathway in the breast cancer pathogenesis. In this study, we found that as compared to the non-tumoral tissues, both C5aR and MAPK/p38 showed an elevated expression, but p21/p-p21 showed lower expression, in the tumoral tissues of breast cancer patients. Mice deficient in C5aR or mice treated with the C5aR antagonist exhibited attenuation of breast cancer growth and reduction in the p38/p-p38 expression, but increase in p21/p-p21 expression, in the tumor tissues. Pre-treatment of the breast cancer cells with recombinant C5a resulted in reduced p21 expression, and MAPK/p38 inhibitors prevented C5a-induced reduction in p21 expression, suggesting the involvement of the MAPK/p38 signaling pathway in the C5a/C5aR-mediated suppression of p21/p-p21 expression. These results provide evidence that breast cancer development may rely on C5a/C5aR interaction, for which MAPK/p38 pathway participate in down-regulating the p21 expression. Inhibition of C5a/C5aR pathway is expected to be helpful for the treatment of patients with breast cancer.

Indexed as

p21-Activated Kinasesp38 Mitogen-Activated Protein KinasesAdultAnimalsBreast NeoplasmsCell Line, TumorCellular SenescenceComplement C5aFemaleHumansMAP Kinase Signaling SystemMiceMice, Inbred BALB CMice, KnockoutMiddle AgedMitogen-Activated Protein KinasesC5AR1 protein, humanComplement C5aMitogen-Activated Protein Kinasesp21-Activated Kinasesp38 Mitogen-Activated Protein KinasesReceptor, Anaphylatoxin C5aRecombinant Proteinsbreast cancerC5a/C5aRp21p38

Identifiers

PMID32669478
PMCPMC7425439
OpenAlexW3042358942

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.