Evidence map›Paper›PMID 32395374›Full record

ArticleJournal of breast cancer2020

Myeloid-Derived Suppressor Cells Recruited by Chemokine (C-C Motif) Ligand 3 Promote the Progression of Breast Cancer via Phosphoinositide 3-Kinase-Protein Kinase B-Mammalian Target of Rapamycin Signaling.

Anqi Luo, Min Meng, Guanying Wang, Rui Han, Yujiao Zhang, Xin Jing, Lin Zhao, Shanzhi Gu, Xinhan Zhao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of breast cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Anqi LuoDepartment of Nuclear medicine, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-0942-6687
Min MengDepartment of Oncology, Shandong Provincial Hospital Affiliated with Shandong University, Jinan, China.ORCID 0000-0002-1977-4650
Guanying WangDepartment of Oncology, First Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0002-5868-2943
Rui HanDepartment of Oncology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID 0000-0003-2612-3570
Yujiao ZhangDepartment of Oncology, First Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0002-8820-1602
Xin JingDepartment of Oncology, First Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0002-4671-3706
Lin ZhaoDepartment of Oncology, First Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0002-2852-8558
Shanzhi GuDepartment of Forensic Medicine, Medical School of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0001-6099-4543
Xinhan ZhaoDepartment of Oncology, First Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0002-8525-4178
First Affiliated Hospital of Xi'an Jiaotong University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFirst Affiliated Hospital of Zhengzhou University · CNShandong Provincial Hospital · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeNumerous studies have shown that the frequency of myeloid-derived suppressor cells (MDSCs) is associated with tumor progression, metastasis, and recurrence. Chemokine (C-C motif) ligand 3 (CCL3) may be secreted by tumor cells and attract MDSCs into the tumor microenvironment. In the present study, we aimed to explore the molecular mechanisms whereby CCL3 is involved in the interaction of breast cancer cells and MDSCs.

methodsThe expression of CCL3 and its receptors was investigated using real-time polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay. The cell counting Kit-8, wound healing, and transwell assays were performed to study cell growth, migration, and invasion. Cell cycling, apoptosis, and the frequency of MDSCs were investigated through flow cytometry. Transwell assays were used for co-culture and chemotaxis detection. Markers of the epithelial-mesenchymal transition (EMT) were determined with western blotting. The role of CCL3

resultsCCL3 promoted cell proliferation, migration, invasion, and cycling, and inhibited apoptosis of breast cancer cells

conclusionCCL3 promoted the growth of breast cancer cells, and MDSCs recruited by CCL3 interacted with these cells and then activated the PI3K-Akt-mTOR pathway, which led to EMT and promoted the migration and invasion of the cells.

Indexed as

Breast neoplasmsChemokine CCL3Epithelial-mesenchymal transitionMyeloid-derived suppressor cellsTumor microenvironment

Identifiers

PMID32395374
PMCPMC7192746
OpenAlexW4238298945

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.