Abstract
Anticancer properties of non-psychoactive cannabinoid cannabidiol (CBD) have been demonstrated on tumors of different histogenesis. Different molecular targets for CBD were proposed, including cannabinoid receptors and some plasma membrane ion channels. Here we have shown that cell lines derived from acute lymphoblastic leukemia of T lineage (T-ALL), but not resting healthy T cells, are highly sensitive to CBD treatment. CBD effect does not depend on cannabinoid receptors or plasma membrane Ca2+-permeable channels. Instead, CBD directly targets mitochondria and alters their capacity to handle Ca2+. At lethal concentrations, CBD causes mitochondrial Ca2+ overload, stable mitochondrial transition pore formation and cell death. Our results suggest that CBD is an attractive candidate to be included into chemotherapeutic protocols for T-ALL treatment.
Highlights
Acute lymphoblastic leukemia (ALL) of T lineage (T-ALL) represents a highly aggressive cancer, resistant to chemotherapy and with increased risk of relapse, which occurs in 15% of childhood and 25% of adult ALL cases
In the present study we addressed the immediate targets for CBD in leukemic cell lines, derived from T-ALL patients in relapse
CBD suppresses viability and impairs migration of leukemic T cells Cytotoxic effect of CBD was first evaluated in leukemic cell lines of different lineages, including T-ALL, B lineage
Summary
Acute lymphoblastic leukemia (ALL) of T lineage (T-ALL) represents a highly aggressive cancer, resistant to chemotherapy and with increased risk of relapse, which occurs in 15% of childhood and 25% of adult ALL cases. G–i Cell death was evaluation by flow cytometry (g, h) and fluorescent microscopy (I) in Jurkat cells treated with different concentrations of CBD using Annexin V-AF488/PI double staining.
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