Evidence map›Paper›PMID 28713975›Full record

ArticleOncology reports2017

CCL28 promotes breast cancer growth and metastasis through MAPK-mediated cellular anti-apoptosis and pro-metastasis.

Xiao Li Yang, Kai Yi Liu, Feng Juan Lin, Hui Min Shi, Zhou Luo Ou

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.4field-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

46 citing papers in PubMed, 75 citations in OpenAlex.

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  8. An Increase in the Chemokine Mediators (CCL28 and CCR10) Associated with the Progression of Oral Squamous Cell Carcinoma: A Cross-Sectional Investigation.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2024
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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

5 authors at 3 institutions in 1 country.

Xiao Li YangBreast Cancer Institute, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Kai Yi LiuDepartment of Biology, College of Life and Environmental Sciences, Shanghai Normal University, Shanghai 200234, P.R. China.
Feng Juan LinBreast Cancer Institute, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Hui Min ShiDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China.
Zhou Luo OuBreast Cancer Institute, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CNShanghai Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is one of the most commonly diagnosed cancers worldwide and the second leading cause of cancer-related deaths among females. CCL28 (mucosa-associated epithelial chemokine, MEC), a CC subfamily chemokine, has been well studied in the process of inflammation, and recently increasing evidence indicates that CCL28 is related to tumor progression. However, little is known concerning its function in breast cancer. In the present study, we generated a CCL28-overexpressing breast cancer cell line MDA-MB-231HM/CCL28 from parental MDA-MB‑231HM cells. We found that overexpression of CCL28 promoted cell proliferation and tumor formation, and also enhanced migration, invasion and metastasis both in vitro and in vivo. Mechanistic studies revealed that CCL28 mediated intracellular activation of the mitogen-activated protein kinase (MAPK) signaling pathway to promote breast cancer cell proliferation and metastasis by upregulating anti-apoptotic protein Bcl-2 and suppressing cell adhesion protein β-catenin. However, overexpression of CCL28 did not influence the expression of metastasis‑related protein matrix metalloproteinase MMP2 and MMP9 and VEGF. Tissue sample analysis from animal models also indicated that overexpression of CCL28 was associated with enhanced pERK expression and reduced β-catenin expression in breast carcinomas. Thus, our results show for the first time that CCL28 contributes to breast cancer progression through the ERK/MAPK‑mediated anti-apoptotic and metastatic signaling pathway. Antagonists of CCL28 and the MAPK signaling pathway may be used synergistically to treat breast cancer patients.

Indexed as

AnimalsApoptosisBiomarkers, TumorBreast NeoplasmsCell AdhesionCell MovementCell ProliferationChemokines, CCFemaleGene Expression Regulation, NeoplasticHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9MCF-7 CellsMiceMitogen-Activated Protein Kinase KinasesBiomarkers, TumorCCL28 protein, humanChemokines, CCMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein Kinase KinasesMMP2 protein, humanMMP9 protein, human

Identifiers

PMID28713975
PMCPMC5549038
OpenAlexW2731059153

What OpenQuestion holds

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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.