Molecular heterogeneity in breast carcinoma cells with increased invasive capacities
Artikel-Kategorie: Research Article
Online veröffentlicht: 14. Feb. 2020
Seitenbereich: 103 - 118
Eingereicht: 10. Jan. 2020
Akzeptiert: 30. Jan. 2020
DOI: https://doi.org/10.2478/raon-2020-0007
Schlüsselwörter
© 2020 Giulia Negro, Bertram Aschenbrenner, Simona Kranjc Brezar, Maja Cemazar, Andrej Coer, Gorana Gasljevic, Dragana Savic, Maxim Sorokin, Anton Buzdin, Maurizio Callari, Irma Kvitsaridze, Anahid Jewett, Mariela Vasileva-Slaveva, Ute Ganswindt, Ira Skvortsova, Sergej Skvortsov, published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.
Background
Metastatic progression of breast cancer is still a challenge in clinical oncology. Therefore, an elucidation how carcinoma cells belonging to different breast cancer subtypes realize their metastatic capacities is needed. The aim of this study was to elucidate a similarity of activated molecular pathways underlying an enhancement of invasiveness of carcinoma cells belonging to different breast carcinoma subtypes.
Materials and methods
In order to reach this aim, parental and invasive (INV) MDA-MB-231 (triple-negative), T47D (hormone receptor-positive), and Au565 (Her2-positive) breast carcinoma cells were used and their molecular phenotypes were compared using a proteomic approach.
Results
Independently from breast cancer subtypes, INV cells have demonstrated fibroblast-like morphology accompanied by enhancement of invasive and migratory capacities, increased expression of cancer stem cell markers, and delayed tumor growth in
Conclusions
We can conclude that hormone receptor-positive cells with increased invasiveness acquire the molecular characteristics of triple-negative breast cancer cells, whereas Her2-positive INV cells specifically changed their own molecular phenotype with very limited partaking in the involved pathways found in the MDA-MB-231-INV and T47D-INV cells. Since hormone receptor-positive invasive cells share their molecular properties with triple-negative breast cancer cells, we assume that these types of metastatic disease can be treated rather equally with an option to add anti-hormonal agents. In contrast, Her2-positive metastasis should be carefully evaluated for more effective therapeutic approaches which are distinct from the triple-negative and hormone-positive metastatic breast cancers.