Simvastatin is effective in killing the radioresistant breast carcinoma cells.


Journal

Radiology and oncology
ISSN: 1581-3207
Titre abrégé: Radiol Oncol
Pays: Poland
ID NLM: 9317213

Informations de publication

Date de publication:
04 05 2021
Historique:
received: 10 03 2021
accepted: 02 04 2021
pubmed: 4 5 2021
medline: 21 9 2021
entrez: 3 5 2021
Statut: epublish

Résumé

Statins, small molecular 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, are widely used to lower cholesterol levels in lipid-metabolism disorders. Recent preclinical and clinical studies have shown that statins exert beneficial effects in the management of breast cancer by increasing recurrence free survival. Unfortunately, the underlying mechanisms remain elusive. Simvastatin, one of the most widely prescribed lipophilic statins was utilized to investigate potential radiosensitizing effects and an impact on cell survival and migration in radioresistant breast cancer cell lines. Compared to parental cell counterparts, radioresistant MDA-MB-231-RR, T47D-RR andAu565-RR cells were characterized by upregulation of 3-hydroxy-3-methylglutharyl-coenzyme A reductase (HMGCR) expression accompanied by epithelial-to-mesenchymal transition (EMT) activation. Radioresistant breast cancer cells can be killed by simvastatin via mobilizing of a variety of pathways involved in apoptosis and autophagy. In the presence of simvastatin migratory abilities and vimentin expression is diminished while E-cadherin expression is increased. The present study suggests that simvastatin may effectively eradicate radioresistant breast carcinoma cells and diminish their mesenchymal phenotypes.

Sections du résumé

BACKGROUND
Statins, small molecular 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, are widely used to lower cholesterol levels in lipid-metabolism disorders. Recent preclinical and clinical studies have shown that statins exert beneficial effects in the management of breast cancer by increasing recurrence free survival. Unfortunately, the underlying mechanisms remain elusive.
MATERIALS AND METHODS
Simvastatin, one of the most widely prescribed lipophilic statins was utilized to investigate potential radiosensitizing effects and an impact on cell survival and migration in radioresistant breast cancer cell lines.
RESULTS
Compared to parental cell counterparts, radioresistant MDA-MB-231-RR, T47D-RR andAu565-RR cells were characterized by upregulation of 3-hydroxy-3-methylglutharyl-coenzyme A reductase (HMGCR) expression accompanied by epithelial-to-mesenchymal transition (EMT) activation. Radioresistant breast cancer cells can be killed by simvastatin via mobilizing of a variety of pathways involved in apoptosis and autophagy. In the presence of simvastatin migratory abilities and vimentin expression is diminished while E-cadherin expression is increased.
CONCLUSIONS
The present study suggests that simvastatin may effectively eradicate radioresistant breast carcinoma cells and diminish their mesenchymal phenotypes.

Identifiants

pubmed: 33939900
pii: raon-2021-0020
doi: 10.2478/raon-2021-0020
pmc: PMC8366725
doi:

Substances chimiques

Cadherins 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
Radiation-Sensitizing Agents 0
Simvastatin AGG2FN16EV
HMGCR protein, human EC 1.1.1.-
Hydroxymethylglutaryl CoA Reductases EC 1.1.1.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

305-316

Informations de copyright

© 2021 Bertram Aschenbrenner, Giulia Negro, Dragana Savic, Maxim Sorokin, Anton Buzdin, Ute Ganswindt, Maja Cemazar, Gregor Sersa, Sergej Skvortsov, Ira Skvortsova, published by Sciendo.

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Auteurs

Bertram Aschenbrenner (B)

Medical University of Innsbruck, Therapeutic Radiology and Oncology, Innsbruck, Austria.
Tyrolean Cancer Research Institute, Innsbruck, Austria.
EORTC PathoBiology Group Moscow, Russia.

Giulia Negro (G)

Medical University of Innsbruck, Therapeutic Radiology and Oncology, Innsbruck, Austria.
Tyrolean Cancer Research Institute, Innsbruck, Austria.
EORTC PathoBiology Group Moscow, Russia.

Dragana Savic (D)

Medical University of Innsbruck, Therapeutic Radiology and Oncology, Innsbruck, Austria.
Tyrolean Cancer Research Institute, Innsbruck, Austria.
EORTC PathoBiology Group Moscow, Russia.

Maxim Sorokin (M)

EORTC PathoBiology Group Moscow, Russia.
Institute of Personalized Medicine, Sechenov First Moscow State Medical University, Moscow, Russia.
Omicsway Corp., Walnut, USA.
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russia.

Anton Buzdin (A)

EORTC PathoBiology Group Moscow, Russia.
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russia.
Oncobox ltd., Moscow, Russia.
World-Class Research Center "Digital Biodesign and Personalized Healthcare", Sechenov First Moscow State Medical University, Moscow, Russia.

Ute Ganswindt (U)

Medical University of Innsbruck, Therapeutic Radiology and Oncology, Innsbruck, Austria.

Maja Cemazar (M)

EORTC PathoBiology Group Moscow, Russia.
Institute of Oncology Ljubljana, Department of Experimental Oncology, Ljubljana, Slovenia.

Gregor Sersa (G)

Institute of Oncology Ljubljana, Department of Experimental Oncology, Ljubljana, Slovenia.

Sergej Skvortsov (S)

Medical University of Innsbruck, Therapeutic Radiology and Oncology, Innsbruck, Austria.
Tyrolean Cancer Research Institute, Innsbruck, Austria.

Ira Skvortsova (I)

Medical University of Innsbruck, Therapeutic Radiology and Oncology, Innsbruck, Austria.
Tyrolean Cancer Research Institute, Innsbruck, Austria.
EORTC PathoBiology Group Moscow, Russia.

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