MEK and MCL-1 sequential inhibition synergize to enhance rhabdomyosarcoma treatment


Por: Alcon C, Martín F, Prada-Varela E, Mora J, Soriano A, Guillén G, Gallego S, Roma J, Samitier J, Villanueva A and Montero J

Publicada: 7 abr 2022 Ahead of Print: 7 abr 2022
Resumen:
Targeted agents have emerged as promising molecules for cancer treatment, but most of them fail to achieve complete tumor regression or attain durable remissions due to tumor adaptations. We used dynamic BH3 profiling to identify targeted agents effectiveness and anti-apoptotic adaptations upon targeted treatment in rhabdomyosarcoma. We focused on studying the use of BH3 mimetics to specifically inhibit pro-survival BCL-2 family proteins, overwhelm resistance to therapy and prevent relapse. We observed that the MEK1/2 inhibitor trametinib rapidly depleted the pro-apoptotic protein NOXA, thus increasing MCL-1 availability. Indeed, we found that the MCL-1 inhibitor S63845 synergistically enhanced trametinib cytotoxicity in rhabdomyosarcoma cells in vitro and in vivo. In conclusion, our findings indicate that the combination of a BH3 mimetic targeting MCL-1 with trametinib improves efficiency on rhabdomyosarcoma by blocking tumor adaptation to treatment.

Filiaciones:
Alcon C:
 Institute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), 08028, Barcelona, Spain

Martín F:
 Institute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), 08028, Barcelona, Spain

 Networking Biomedical Research Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28029, Madrid, Spain

Prada-Varela E:
 Developmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, 08950, Esplugues de Llobregat, Spain

 Pediatric Cancer Center Barcelona (PCCB), Hospital Sant Joan de Déu Barcelona, 08950, Esplugues de Llobregat, Spain

Mora J:
 Developmental Tumor Biology Laboratory, Institut de Recerca Sant Joan de Déu, 08950, Esplugues de Llobregat, Spain

Soriano A:
 Group of Translational Research in Child and Adolescent Cancer, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), 08035, Barcelona, Spain

Guillén G:
 Group of Translational Research in Child and Adolescent Cancer, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), 08035, Barcelona, Spain

 Department of Surgery, Universitat Autònoma de Barcelona (UAB), 08193, Barcelona, Spain

Gallego S:
 Group of Translational Research in Child and Adolescent Cancer, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), 08035, Barcelona, Spain

Roma J:
 Group of Translational Research in Child and Adolescent Cancer, Vall d'Hebron Research Institute (VHIR), Universitat Autònoma de Barcelona (UAB), 08035, Barcelona, Spain

Samitier J:
 Institute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), 08028, Barcelona, Spain

 Networking Biomedical Research Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28029, Madrid, Spain

 Department of Electronics and Biomedical Engineering, University of Barcelona (UB), 08028, Barcelona, Spain

Villanueva A:
 Program against Cancer Therapeutic Resistance (ProCURE), IDIBELL, Catalan Institute of Oncology, 08907 l'Hospitalet del Llobregat, Barcelona, Spain

 Xenopat S.L., Business Bioincubator, Bellvitge Health Science Campus, 08907 l'Hospitalet de Llobregat, Barcelona, Spain

Montero J:
 Institute for Bioengineering of Catalonia (IBEC), Barcelona Institute of Science and Technology (BIST), 08028, Barcelona, Spain.

 Networking Biomedical Research Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 28029, Madrid, Spain.
ISSN: 20587716





Cell Death Discovery
Editorial
SPRINGERNATURE, CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND, Reino Unido
Tipo de documento: Article
Volumen: 8 Número: 1
Páginas: 172-172
WOS Id: 000779755500001
ID de PubMed: 35393436
imagen Green Submitted, gold

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