Navitoclax combined with Alpelisib effectively inhibits Merkel cell carcinoma cell growth

BCL-2 inhibitor Merkel cell carcinoma Merkel cell polyomavirus PI3K inhibitor apoptosis

Journal

Therapeutic advances in medical oncology
ISSN: 1758-8340
Titre abrégé: Ther Adv Med Oncol
Pays: England
ID NLM: 101510808

Informations de publication

Date de publication:
2020
Historique:
received: 23 07 2020
accepted: 29 10 2020
entrez: 6 1 2021
pubmed: 7 1 2021
medline: 7 1 2021
Statut: epublish

Résumé

Merkel cell carcinoma (MCC) is a highly malignant skin cancer. Despite major treatment improvements during the last decade, up to 50% of patients do not respond to therapy or develop recurrent disease. For these patients, alternative treatment options are urgently needed. Here, we assessed the efficacy of the combination of the BCL-2 inhibitor Navitoclax and the PI3K p110α inhibitor Alpelisib in MCC cell lines. The expression of BCL-2 was assessed by immunohistochemistry in MCC and MCC cell lines. Treatment with Navitoclax and Alpelisib alone and in combination was performed on four MCC cell lines. The decrease of cell viability during treatment was assessed by XTT assay and visualized for the combinations by 3D combinatorial index plotting. The increase of apoptotic cells was determined by cleaved PARP Western blotting and Annexin V staining. Some 94% of MCCs and all three MCPyV-positive cell lines showed BCL-2 expression. Navitoclax monotreatment was shown to be highly effective when treating BCL-2-positive cell lines (IC Our results show that the anti-apoptotic BCL-2 is frequently expressed in MCC and MCC cell lines. Inhibition of BCL-2 by Navitoclax in combination with Alpelisib revealed a strong synergy and prolonged inhibition of MCC cell viability and induction of apoptosis. The combination of Navitoclax and Alpelisib is a novel potential treatment option for MCC patients.

Sections du résumé

BACKGROUND BACKGROUND
Merkel cell carcinoma (MCC) is a highly malignant skin cancer. Despite major treatment improvements during the last decade, up to 50% of patients do not respond to therapy or develop recurrent disease. For these patients, alternative treatment options are urgently needed. Here, we assessed the efficacy of the combination of the BCL-2 inhibitor Navitoclax and the PI3K p110α inhibitor Alpelisib in MCC cell lines.
METHODS METHODS
The expression of BCL-2 was assessed by immunohistochemistry in MCC and MCC cell lines. Treatment with Navitoclax and Alpelisib alone and in combination was performed on four MCC cell lines. The decrease of cell viability during treatment was assessed by XTT assay and visualized for the combinations by 3D combinatorial index plotting. The increase of apoptotic cells was determined by cleaved PARP Western blotting and Annexin V staining.
RESULTS RESULTS
Some 94% of MCCs and all three MCPyV-positive cell lines showed BCL-2 expression. Navitoclax monotreatment was shown to be highly effective when treating BCL-2-positive cell lines (IC
DISCUSSION CONCLUSIONS
Our results show that the anti-apoptotic BCL-2 is frequently expressed in MCC and MCC cell lines. Inhibition of BCL-2 by Navitoclax in combination with Alpelisib revealed a strong synergy and prolonged inhibition of MCC cell viability and induction of apoptosis. The combination of Navitoclax and Alpelisib is a novel potential treatment option for MCC patients.

Identifiants

pubmed: 33403016
doi: 10.1177/1758835920975621
pii: 10.1177_1758835920975621
pmc: PMC7739210
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1758835920975621

Informations de copyright

© The Author(s), 2020.

Déclaration de conflit d'intérêts

Declaration of conflicting interest: The authors declare that there is no conflict of interest.

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Auteurs

Emil Chteinberg (E)

Department of Pathology, GROW-School for Oncology and Developmental Biology, Maastricht University Medical Centre+, Maastricht, Limburg, The Netherlands.

Suzan Wetzels (S)

Experimental Vascular Pathology, Department of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Limburg, The Netherlands.

Wouter Gerritsen (W)

Department of Pathology, GROW-School for Oncology and Developmental Biology, Maastricht University Medical Centre+, Maastricht, Limburg, The Netherlands.

Lieve Temmerman (L)

Experimental Vascular Pathology, Department of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Limburg, The Netherlands.

Joost van den Oord (J)

Laboratory of Translational Cell and Tissue Research, University of Leuven, Leuven.

Erik Biessen (E)

Experimental Vascular Pathology, Department of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Limburg, The Netherlands.

Anna Kordelia Kurz (AK)

Department of Internal Medicine IV, RWTH Aachen University Hospital, Aachen, Nordrhein-Westfalen, Germany.

Véronique Winnepenninckx (V)

Department of Pathology, GROW-School for Oncology and Developmental Biology, Maastricht University Medical Centre+, Maastricht, Limburg, The Netherlands.

Martin Zenke (M)

Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University Hospital, Aachen, Nordrhein-Westfalen, Germany.

Ernst-Jan Speel (EJ)

Department of Pathology, GROW-School for Oncology and Developmental Biology, Maastricht University Medical Centre+, Maastricht, Limburg, The Netherlands.

Axel Zur Hausen (A)

Department of Pathology, GROW-School for Oncology and Developmental Biology, Maastricht University Medical Centre +, P. Debyelaan 25, Maastricht, 6229 HX, The Netherlands.

Classifications MeSH