Apoptotic and Non-Apoptotic Modalities of Thymoquinone-Induced Lymphoma Cell Death: Highlight of the Role of Cytosolic Calcium and Necroptosis.
ER-stress
apoptosis
diffuse large B cell lymphoma (DLBCL)
necroptosis
non-apoptotic cell death
thymoquinone
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
16 Jul 2021
16 Jul 2021
Historique:
received:
15
05
2021
revised:
08
07
2021
accepted:
09
07
2021
entrez:
24
7
2021
pubmed:
25
7
2021
medline:
25
7
2021
Statut:
epublish
Résumé
Targeting non-apoptotic modalities might be therapeutically promising in diffuse large B cell lymphoma (DLBCL) patients with compromised apoptotic pathways. Thymoquinone (TQ) has been reported to promote apoptosis in cancer cells, but little is known about its effect on non-apoptotic pathways. This work investigates TQ selectivity against DLBCL cell lines and the cell death mechanisms. TQ reduces cell viability and kills cell lines with minimal toxicity on normal hematological cells. Mechanistically, TQ promotes the mitochondrial caspase pathway and increases genotoxicity. However, insensitivity of most cell lines to caspase inhibition by z-VAD-fmk (benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone) pointed to a critical role of non-apoptotic signaling. In cells dying through non-apoptotic death, TQ increases endoplasmic reticulum (ER) stress markers and substantially increases cytosolic calcium ([Ca
Identifiants
pubmed: 34298792
pii: cancers13143579
doi: 10.3390/cancers13143579
pmc: PMC8304872
pii:
doi:
Types de publication
Journal Article
Langues
eng
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