Evidence map›Paper›PMID 26487662›Full record

ArticleMedical oncology (Northwood, London, England)2015

The human chemokine receptor CCRL2 suppresses chemotaxis and invasion by blocking CCL2-induced phosphorylation of p38 MAPK in human breast cancer cells.

Lei-Ping Wang, Jun Cao, Jian Zhang, Bi-Yun Wang, Xi-Chun Hu, Zhi-Min Shao, Zhong-Hua Wang, Zhou-Luo Ou

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  10. Review
  11. Molecular Basis for CCRL2 Regulation of Leukocyte Migration.Frontiers in cell and developmental biology · 2020
    Review
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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

8 authors at 2 institutions in 1 country.

Lei-Ping WangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China.
Jun CaoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China.
Jian ZhangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China.
Bi-Yun WangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China.
Xi-Chun HuDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China.
Zhi-Min ShaoDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China.
Zhong-Hua WangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China. wzzhuaw_2015@126.com.
Zhou-Luo OuDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, 270 Dongan Road, Shanghai, China. wzzhuaw@163.com.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human chemokine receptor CCRL2 is a member of the atypical chemokine receptor family. CCRL2 is unable to couple with G-proteins and fails to induce classical chemokine signaling for the highly conserved DRYLAIV motif essential for signaling has been changed to QRYLVFL. We investigated whether CCRL2 is involved in the chemotaxis, invasion, and proliferation of human breast cancer cells. Firstly, expression of CCRL2 was determined in six breast cancer cell lines by real-time RT-PCR and Western blot. Then, we established stable cell lines overexpressing CCRL2 to explore the function of CCRL2 in chemotaxis and invasion by transwell assays, and the signaling downstream was further investigated. The effect of CCRL2 on proliferation was detected by colony formation assays and tumor xenograft study. We found that stable overexpression of CCRL2 in MDA-MB-231 and BT-549 cells attenuated the chemotaxis and invasion stimulated by its ligand CCL2. CCRL2 inhibits p38 MAPK (p38) phosphorylation and up-regulates the expression of E-cadherin. This effect was eliminated by the inhibitor of p38 MAPK. CCRL2 inhibited the growth of breast cancer cells in vitro and in vivo. Our results suggest that CCRL2 functions as a tumor suppressor in human breast cancer cells.

Indexed as

Breast NeoplasmsCell Line, TumorChemokine CCL2ChemotaxisFemaleHumansMCF-7 CellsNeoplasm Invasivenessp38 Mitogen-Activated Protein KinasesPhosphorylationReceptors, CCRCCL2 protein, humanCCRL2 protein, humanChemokine CCL2p38 Mitogen-Activated Protein KinasesReceptors, CCRBreast cancerCCL2CCRL2ChemotaxisInvasionp38 MAPK

Identifiers

PMID26487662
OpenAlexW2173035379

What OpenQuestion holds

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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.