Evidence map›Paper›PMID 25744294›Full record

ArticleBreast cancer research and treatment2015

The CCL2 chemokine is a negative regulator of autophagy and necrosis in luminal B breast cancer cells.

Wei Bin Fang, Min Yao, Iman Jokar, Nabil Alhakamy, Cory Berkland, Jin Chen, Dana Brantley-Sieders, Nikki Cheng

Open access · greenAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

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  20. Elevated expression of chemokine C-C ligand 2 in stroma is associated with recurrent basal-like breast cancers.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    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

8 authors at 3 institutions in 1 country.

Wei Bin FangDepartment of Pathology and Laboratory, University of Kansas Medical Center, 3901 Rainbow Boulevard, Wahl Hall East 1020, Kansas, KS, 66160, USA.
Min Yao
Iman Jokar
Nabil Alhakamy
Cory Berkland
Jin Chen
Dana Brantley-Sieders
Nikki Cheng
University of Kansas Medical Center · USUniversity of Kansas · USVanderbilt University Medical Center · US

Funding

Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUTKENHAUS, JOSEPH F · 2012 to 2016
$5.3M
Progression of DCIS to Invasive Breast Cancer through CCR2 Chemokine SignalingR01CA172764 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CHENG, NIKKI · 2013 to 2024
$4.2M
ephrin-A1 in lipogenesis and breast cancer metastatic progressionR01CA177681 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BRANTLEY-SIEDERS, DANA M, CHEN, JIN · 2014 to 2019
$1.9M
Functions of chemokine and TGF-B signaling in the breast cancer microenvironmentR00CA127357 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CHENG, NIKKI · 2010 to 2012
$732k
Functions of chemokine and TGF-B signaling in the breast cancer microenvironmentK99CA127357 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI CHENG, NIKKI · 2008 to 2009
$298k
NCI NIH HHS CA127357NCI NIH HHS K99 CA127357NCI NIH HHS R00 CA127357NCI NIH HHS R01 CA172764NCI NIH HHS R01 CA177681NIGMS NIH HHS P30 GM103326
6 · The paper itself

Abstract

Luminal A and B breast cancers are the most prevalent forms of breast cancer diagnosed in women. Compared to luminal A breast cancer patients, patients with luminal B breast cancers experience increased disease recurrence and lower overall survival. The mechanisms that regulate the luminal B subtype remain poorly understood. The chemokine CCL2 is overexpressed in breast cancer, correlating with poor patient prognosis. The purpose of this study was to determine the role of CCL2 expression in luminal B breast cancer cells. Breast tissues, MMTV-PyVmT and MMTV-Neu transgenic mammary tumors forming luminal B-like lesions, were immunostained for CCL2 expression. To determine the role of CCL2 in breast cancer cells, CCL2 gene expression was silenced in mammary tumor tissues and cells using TAT cell-penetrating peptides non-covalently cross linked to siRNAs (Ca-TAT/siRNA). CCL2 expression was examined by ELISA and flow cytometry. Cell growth and survival were analyzed by flow cytometry, immunocytochemistry, and fluorescence microscopy. CCL2 expression was significantly increased in luminal B breast tumors, MMTV- PyVmT and MMTV-Neu mammary tumors, compared or normal breast tissue or luminal A breast tumors. Ca-TAT delivery of CCL2 siRNAs significantly reduced CCL2 expression in PyVmT mammary tumors, and decreased cell proliferation and survival. CCL2 gene silencing in PyVmT carcinoma cells or BT474 luminal B breast cancer cells decreased cell growth and viability associated with increased necrosis and autophagy. CCL2 expression is overexpressed in luminal B breast cancer cells and is important for regulating cell growth and survival by inhibiting necrosis and autophagy.

Indexed as

AutophagyAnimalsBreast NeoplasmsCarcinoma, Ductal, BreastCell ProliferationCell SurvivalChemokine CCL2FemaleGene ExpressionGene Knockdown TechniquesHumansMCF-7 CellsMiceMice, TransgenicNecrosisRNA, Small InterferingCCL2 protein, humanChemokine CCL2RNA, Small Interfering

Identifiers

PMID25744294
PMCPMC4456035
OpenAlexW2071504859

What OpenQuestion holds

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LicenceTDM
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.