Evidence map›Paper›PMID 27409163›Full record

ArticleOncotarget2016

Salinomycin co-treatment enhances tamoxifen cytotoxicity in luminal A breast tumor cells by facilitating lysosomal degradation of receptor tyrosine kinases.

Ann-Katrin Sommer, Adam Hermawan, Frauke Martina Mickler, Bojan Ljepoja, Pjotr Knyazev, Christoph Bräuchle, Axel Ullrich, Ernst Wagner, Andreas Roidl

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-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

10 citing papers in PubMed, 18 citations in OpenAlex.

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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 2 institutions in 1 country.

Ann-Katrin SommerPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Adam HermawanPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Frauke Martina MicklerPhysical Chemistry, Department of Chemistry, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Bojan LjepojaPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Pjotr KnyazevDepartment of Molecular Biology, Max-Planck-Institute of Biochemistry, 82152 Martinsried, Germany.
Christoph BräuchlePhysical Chemistry, Department of Chemistry, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Axel UllrichDepartment of Molecular Biology, Max-Planck-Institute of Biochemistry, 82152 Martinsried, Germany.
Ernst WagnerPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Andreas RoidlPharmaceutical Biotechnology, Department of Pharmacy, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Ludwig-Maximilians-Universität München · DEMax Planck Institute of Biochemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Luminal A breast cancer is the most common breast cancer subtype which is usually treated with selective estrogen receptor modulators (SERMS) like tamoxifen. Nevertheless, one third of estrogen receptor positive breast cancer patients initially do not respond to endocrine therapy and about 40% of luminal A breast tumors recur in five years. In this study, we investigated an alternative treatment approach by combining tamoxifen and salinomycin in luminal A breast cancer cell lines. We have found that salinomycin induces an additional cytotoxic effect by inhibiting the ligand independent activation of ERα. Thereby salinomycin increases the intracellular calcium level. This leads to a premature fusion of endosomes with lysosomes and thus to the degradation of Egfr family members. Since this process is essential for luminal A breast cancer cells to circumvent tamoxifen treatment, the combination of both drugs induces cytotoxicity in tamoxifen sensitive as well as resistant luminal A breast cancer cell lines.

Indexed as

Biological TransportBreast NeoplasmsCell Line, TumorCell SurvivalDrug Screening Assays, AntitumorDrug SynergismEndosomesEstrogen Receptor alphaFemaleHumansInhibitory Concentration 50LigandsLysosomesMCF-7 CellsPhenobarbitalPolyether PolyketidesESR1 protein, humanEstrogen Receptor alphaLigandsPhenobarbitalPolyether PolyketidesPyransReceptor Protein-Tyrosine KinasessalinomycinSelective Estrogen Receptor ModulatorsTamoxifenbreast cancerendosomal traffickingresistancesalinomycintamoxifen

Identifiers

PMID27409163
PMCPMC5226596
OpenAlexW2467745789

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.