Periplocin mediates TRAIL-induced apoptosis and cell cycle arrest in human myxofibrosarcoma cells via the ERK/p38/JNK pathway.

Apoptosis Death receptors Myxofibrosarcoma Periploca sepium Periplocin

Journal

Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794

Informations de publication

Date de publication:
05 Jun 2020
Historique:
received: 24 02 2020
revised: 26 05 2020
accepted: 03 06 2020
pubmed: 20 6 2020
medline: 20 6 2020
entrez: 20 6 2020
Statut: aheadofprint

Résumé

Periploca sepium is traditionally used in Chinese medicine to treat particularly rheumatic disorders and as a tonic. Periplocin was found as the most cytotoxic compound of its root bark and induced death receptor mediated apoptosis in liposarcoma cells. Sarcomas are a rare type of cancer with only a few treatment options. The five-year survival rate of advanced tumors is low. In this study, we investigated the effects of periplocin in two myxofibrosarcoma (MFS)cell lines, MUG-Myx2a and MUG-Myx2b, which are subclones of the same tumor and reflect the tumor´s heterogeneity, and in T60 primary myxofibrosarcoma cells. The xCELLigence system and the CellTiter 96® AQ Periplocin decreased dose-dependently the viability of all MFS cell lines and was more effective than the standard chemotherapeutic doxorubicin. It arrested the cells in the G2/M phase and led to caspase activation. Moreover, periplocin increased the mRNA expression of NOXA, Bak, Bcl-2, and death receptors such as TRAIL-R1 and TRAIL-R2 and the protein expression of ERK/phospho ERK, p38/phospho p38, and JNK/phospho JNK. In all cases, differences in the effects in the different subclones were observed. Periplocin showed promising effects in MFS cells. The higher effectiveness compared to doxorubicin is an important aspect for further research with regard as a treatment option. The different effects of periplocin in the two subclones showed the great importance of intratumoral heterogeneity in MFS therapy.

Sections du résumé

BACKGROUND BACKGROUND
Periploca sepium is traditionally used in Chinese medicine to treat particularly rheumatic disorders and as a tonic. Periplocin was found as the most cytotoxic compound of its root bark and induced death receptor mediated apoptosis in liposarcoma cells. Sarcomas are a rare type of cancer with only a few treatment options. The five-year survival rate of advanced tumors is low.
PURPOSE OBJECTIVE
In this study, we investigated the effects of periplocin in two myxofibrosarcoma (MFS)cell lines, MUG-Myx2a and MUG-Myx2b, which are subclones of the same tumor and reflect the tumor´s heterogeneity, and in T60 primary myxofibrosarcoma cells.
METHODS METHODS
The xCELLigence system and the CellTiter 96® AQ
RESULTS RESULTS
Periplocin decreased dose-dependently the viability of all MFS cell lines and was more effective than the standard chemotherapeutic doxorubicin. It arrested the cells in the G2/M phase and led to caspase activation. Moreover, periplocin increased the mRNA expression of NOXA, Bak, Bcl-2, and death receptors such as TRAIL-R1 and TRAIL-R2 and the protein expression of ERK/phospho ERK, p38/phospho p38, and JNK/phospho JNK. In all cases, differences in the effects in the different subclones were observed.
CONCLUSION CONCLUSIONS
Periplocin showed promising effects in MFS cells. The higher effectiveness compared to doxorubicin is an important aspect for further research with regard as a treatment option. The different effects of periplocin in the two subclones showed the great importance of intratumoral heterogeneity in MFS therapy.

Identifiants

pubmed: 32559583
pii: S0944-7113(20)30093-3
doi: 10.1016/j.phymed.2020.153262
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

153262

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier GmbH.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None.

Auteurs

Birgit Lohberger (B)

Department of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5, 8036Graz, Austria. Electronic address: birgit.lohberger@medunigraz.at.

Eva Bernhart (E)

Division of Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstrasse 6/6, 8010Graz, Austria.

Nicole Stuendl (N)

Department of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5, 8036Graz, Austria.

Dietmar Glaenzer (D)

Department of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5, 8036Graz, Austria.

Andreas Leithner (A)

Department of Orthopedics and Trauma, Medical University of Graz, Auenbruggerplatz 5, 8036Graz, Austria.

Beate Rinner (B)

Division of Biomedical Research, Medical University Graz, Roseggerweg 48, 8036Graz, Austria.

Rudolf Bauer (R)

Institute of Pharmaceutical Sciences, Department of Pharmacognosy, University of Graz, Universitaetsplatz 4/1, 8010Graz, Austria.

Nadine Kretschmer (N)

Division of Biomedical Research, Medical University Graz, Roseggerweg 48, 8036Graz, Austria; Institute of Pharmaceutical Sciences, Department of Pharmacognosy, University of Graz, Universitaetsplatz 4/1, 8010Graz, Austria.

Classifications MeSH