Increased MCL1 dependency leads to new applications of BH3-mimetics in drug-resistant neuroblastoma.
Child
Humans
Myeloid Cell Leukemia Sequence 1 Protein
/ metabolism
Proto-Oncogene Proteins
/ metabolism
Cisplatin
/ pharmacology
Cell Line, Tumor
Neoplasm Recurrence, Local
/ drug therapy
Proto-Oncogene Proteins c-bcl-2
/ metabolism
Neuroblastoma
/ drug therapy
Antineoplastic Agents
/ pharmacology
Apoptosis
Journal
British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635
Informations de publication
Date de publication:
11 2023
11 2023
Historique:
received:
14
03
2023
accepted:
06
09
2023
revised:
16
08
2023
medline:
16
11
2023
pubmed:
19
9
2023
entrez:
18
9
2023
Statut:
ppublish
Résumé
Neuroblastoma is a paediatric cancer that is characterised by poor prognosis for chemoresistant disease, highlighting the need for better treatment options. Here, we asked whether BH3-mimetics inhibiting BCL2 proteins may eliminate chemoresistant neuroblastoma cells. We utilised cisplatin-adapted neuroblastoma cell lines as well as patient tissues before and after relapse to study alterations of BCL2 proteins upon chemoresistance. In a direct comparison of cisplatin-resistant cells we identified a prominent loss of sensitivity to BCL2/BCL-X These data highlight that the application of BH3-mimetics may differ between first line treatment and relapsed disease. Combination of NK cell-based immunotherapy with BH3-mimetics may further increase killing of chemoresistant neuroblastoma, outlining a new treatment strategy for relapsed neuroblastoma.
Sections du résumé
BACKGROUND
Neuroblastoma is a paediatric cancer that is characterised by poor prognosis for chemoresistant disease, highlighting the need for better treatment options. Here, we asked whether BH3-mimetics inhibiting BCL2 proteins may eliminate chemoresistant neuroblastoma cells.
METHODS
We utilised cisplatin-adapted neuroblastoma cell lines as well as patient tissues before and after relapse to study alterations of BCL2 proteins upon chemoresistance.
RESULTS
In a direct comparison of cisplatin-resistant cells we identified a prominent loss of sensitivity to BCL2/BCL-X
CONCLUSIONS
These data highlight that the application of BH3-mimetics may differ between first line treatment and relapsed disease. Combination of NK cell-based immunotherapy with BH3-mimetics may further increase killing of chemoresistant neuroblastoma, outlining a new treatment strategy for relapsed neuroblastoma.
Identifiants
pubmed: 37723317
doi: 10.1038/s41416-023-02430-8
pii: 10.1038/s41416-023-02430-8
pmc: PMC10646009
doi:
Substances chimiques
Myeloid Cell Leukemia Sequence 1 Protein
0
Proto-Oncogene Proteins
0
Cisplatin
Q20Q21Q62J
Proto-Oncogene Proteins c-bcl-2
0
Antineoplastic Agents
0
MCL1 protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1667-1678Informations de copyright
© 2023. The Author(s).
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