Evidence map›Paper›PMID 35298675›Full record

ArticleArchives of gynecology and obstetrics2022

Protein kinase C targeting of luminal (T-47D), luminal/HER2-positive (BT474), and triple negative (HCC1806) breast cancer cells in-vitro with AEB071 (Sotrastaurin) is efficient but mediated by subtype specific molecular effects.

Veruschka Albert, Gerhard Piendl, Dali Yousseff, Hedwig Lammert, Michael Hummel, Olaf Ortmann, Wolfgang Jagla, Andreas Gaumann, Anja K Wege, Gero Brockhoff

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of gynecology and obstetrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  5. Article
  6. 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

10 authors at 2 institutions in 1 country.

Veruschka AlbertDepartment of Gynecology and Obstetrics, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.
Gerhard PiendlDepartment of Gynecology and Obstetrics, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.
Dali YousseffInstitute of Pathology, Kaufbeuren, Germany.
Hedwig LammertInstitute of Pathology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Michael HummelInstitute of Pathology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Olaf OrtmannDepartment of Gynecology and Obstetrics, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.
Wolfgang JaglaInstitute of Pathology, Kaufbeuren, Germany.
Andreas GaumannInstitute of Pathology, Kaufbeuren, Germany.
Anja K WegeDepartment of Gynecology and Obstetrics, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.
Gero BrockhoffDepartment of Gynecology and Obstetrics, University Medical Center Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany. gero.brockhoff@ukr.de.ORCID 0000-0001-8398-8349
University Hospital Regensburg · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeProtein kinase C (PKC) plays a pivotal role in malignant cell proliferation, apoptosis, invasiveness and migration. However, its exploitation as therapeutic target in breast cancer has been merely explored. Here were evaluated the AEB071 (Sotrastaurin™) treatment efficiency of breast cancer cell lines derived from estrogen receptor positive (T-47D), estrogen/HER2 receptor positive (BT474), and triple negative (HCC1806) breast cancer cells under 2D (monolayer) and 3D (multicellular tumor spheroids) culture conditions. Additionally, spheroid cocultures of BC and N1 fibroblasts were analyzed.

methodsWe quantitatively assessed the proliferation capacity of breast cancer cells and fibroblasts as a function of AEB071 treatment using flow cytometry. The activities of PKC isoforms, substrates, and key molecules of the PKC signaling known to be involved in the regulation of tumor cell proliferation and cellular survival were additionally evaluated. Moreover, a multigene expression analysis (PanCancer Pathways assay) using the nanoString™ technology was applied.

resultsAll breast cancer cell lines subjected to this study were sensitive to AEB071 treatment, whereby cell proliferation in 2D culture was considerably (BT474) or moderately (HCC1806) retarded in G0/G1 or in G2/M phase (T-47D) of the cell cycle. Regardless of the breast cancer subtype the efficiency of AEB071 treatment was significantly lower in the presence of N1 fibroblast cells. Subtype specific driver molecules, namely IL19, c-myb, and NGFR were mostly affected by the AEB071 treatment.

conclusionA combined targeting of PKC and a subtype specific driver molecule might complement specified breast cancer treatment.

Indexed as

Breast NeoplasmsProtein Kinase CCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleHumansPyrrolesQuinazolinesErb-b2 Receptor Tyrosine KinasesProtein Kinase CPyrrolesQuinazolinessotrastaurinAEB071Breast cancerProtein kinase CSotrastaurin

Identifiers

PMID35298675
PMCPMC9470618
OpenAlexW4221026062

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.