Overexpression of Prolidase Induces Autophagic Death in MCF-7 Breast Cancer Cells.


Journal

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
ISSN: 1421-9778
Titre abrégé: Cell Physiol Biochem
Pays: Germany
ID NLM: 9113221

Informations de publication

Date de publication:
12 Sep 2020
Historique:
accepted: 02 09 2020
entrez: 12 9 2020
pubmed: 13 9 2020
medline: 26 1 2021
Statut: ppublish

Résumé

Proline availability for proline dehydrogenase/proline oxidase (PRODH/POX) may represent switching mechanism between PRODH/POX-dependent apoptosis and autophagy. The aim of the study was to evaluate the impact of overexpression of prolidase (proline releasing enzyme) on apoptosis/autophagy in breast cancer MCF-7 cells. The model of MCF-7 cells with prolidase overexpression (MCF-7 Prolidase overexpression in MCF-7 The data suggest that overexpression of prolidase in MCF-7 cells contributes to increase in intracellular proline concentration and PRODH/POX-dependent autophagic cell death.

Sections du résumé

BACKGROUND/AIMS OBJECTIVE
Proline availability for proline dehydrogenase/proline oxidase (PRODH/POX) may represent switching mechanism between PRODH/POX-dependent apoptosis and autophagy. The aim of the study was to evaluate the impact of overexpression of prolidase (proline releasing enzyme) on apoptosis/autophagy in breast cancer MCF-7 cells.
METHODS METHODS
The model of MCF-7 cells with prolidase overexpression (MCF-7
RESULTS RESULTS
Prolidase overexpression in MCF-7
CONCLUSION CONCLUSIONS
The data suggest that overexpression of prolidase in MCF-7 cells contributes to increase in intracellular proline concentration and PRODH/POX-dependent autophagic cell death.

Identifiants

pubmed: 32918543
doi: 10.33594/000000275
doi:

Substances chimiques

Collagen 9007-34-5
Proline 9DLQ4CIU6V
Proline Oxidase EC 1.5.3.-
Dipeptidases EC 3.4.13.-
proline dipeptidase EC 3.4.13.9

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

875-887

Subventions

Organisme : National Science Center (NCN)
ID : 2017/25/B/NZ7/02183
Pays : Poland
Organisme : The European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant and the Polish Ministry of Science and Higher Education, from financial resources for science in 2018-2023 granted for the implementation of an international co-financed project
Pays : Poland

Informations de copyright

© Copyright by the Author(s). Published by Cell Physiol Biochem Press.

Déclaration de conflit d'intérêts

The authors have no conflicts of interest to declare.

Auteurs

Ilona Zareba (I)

Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland.

Thi Yen Ly Huynh (TYL)

Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland.

Adam Kazberuk (A)

Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland.

Joanna Teul (J)

Department of Pharmaceutical and Biopharmaceutical Analysis, Medical University of Bialystok, Bialystok, Poland.

Agnieszka Klupczynska (A)

Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland.
Department of Inorganic and Analytical Chemistry, Poznan University of Medical Sciences, Poznan, Poland.

Jan Matysiak (J)

Department of Inorganic and Analytical Chemistry, Poznan University of Medical Sciences, Poznan, Poland.

Arkadiusz Surazynski (A)

Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland.

Jerzy Palka (J)

Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland, pal@umb.edu.pl.

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Classifications MeSH