Evidence map›Paper›PMID 26158518›Full record

ArticleCell death & disease2015

Estrogen receptor α regulates non-canonical autophagy that provides stress resistance to neuroblastoma and breast cancer cells and involves BAG3 function.

V Felzen, C Hiebel, I Koziollek-Drechsler, S Reißig, U Wolfrum, D Kögel, C Brandts, C Behl, T Morawe

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 78 citations in OpenAlex.

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  8. BAG family proteins contributes to autophagy-mediated multidrug resistance of tumor.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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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

9 authors at 4 institutions in 1 country.

V FelzenInstitute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
C HiebelInstitute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
I Koziollek-DrechslerInstitute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
S ReißigInstitute of Molecular Medicine, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
U WolfrumDepartment of Cell and Matrix Biology, Institute of Zoology, Johannes Gutenberg University Mainz, Mainz, Germany.
D KögelExperimental Neurosurgery, Neuroscience Center, Goethe University Hospital, Frankfurt, Germany.
C BrandtsDepartment of Medicine, Hematology/Oncology and University Cancer Center Frankfurt, Goethe University Hospital, Frankfurt, Germany.
C BehlInstitute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
T MoraweInstitute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEFrankfurt Cancer Institute · DEUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is a heterogeneous disease and approximately 70% of newly diagnosed breast cancers are estrogen receptor (ER) positive. Out of the two ER types, α and β, ERα is the only ER that is detectable by immunohistochemistry in breast cancer biopsies and is the predominant subtype expressed in breast tumor tissue. ER-positive tumors are currently treated with anti-hormone therapy to inhibit ER signaling. It is well known that breast cancer cells can develop endocrine resistance and resistance to anti-hormone therapy and this can be facilitated via the autophagy pathway, but so far the description of a detailed autophagy expression profile of ER-positive cancer cells is missing. In the present study, we characterized tumor cell lines ectopically expressing ERα or ERβ as well as the breast cancer-derived MCF-7 cell line endogenously expressing ERα but being ERβ negative. We could show that ERα-expressing cells have a higher autophagic activity than cells expressing ERβ and cells lacking ER expression. Additionally, for autophagy-related gene expression we describe an ERα-specific 'autophagy-footprint' that is fundamentally different to tumor cells expressing ERβ or lacking ER expression. This newly described ERα-mediated and estrogen response element (ERE)-independent non-canonical autophagy pathway, which involves the function of the co-chaperone Bcl2-associated athanogene 3 (BAG3), is independent of classical mammalian target of rapamycin (mTOR) and phosphatidylinositol 3 kinase (PI3K) signaling networks and provides stress resistance in our model systems. Altogether, our study uncovers a novel non-canonical autophagy pathway that might be an interesting target for personalized medicine and treatment of ERα-positive breast cancer cells that do not respond to anti-hormone therapy and classical autophagy inhibitors.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsAutophagyBreast NeoplasmsEstrogen Receptor alphaEstrogen Receptor betaEstrogen Replacement TherapyFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsNeuroblastomaPrecision MedicineSignal TransductionAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBAG3 protein, humanEstrogen Receptor alphaEstrogen Receptor beta

Identifiers

PMID26158518
PMCPMC4650728
OpenAlexW810230962

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.