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Δ 9 ‐Tetrahydrocannabinol induces apoptosis in C6 glioma cells
Author(s) -
Sánchez Cristina,
Galve-Roperh Ismael,
Canova Cecile,
Brachet Philippe,
Guzmán Manuel
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01085-0
Subject(s) - cannabinoid receptor , apoptosis , sphingomyelin , ceramide , cannabinoid , glioma , chemistry , dna fragmentation , microbiology and biotechnology , tetrahydrocannabinol , biology , receptor , biochemistry , programmed cell death , antagonist , cancer research , membrane
Δ 9 ‐Tetrahydrocannabinol (THC), the major active component of marijuana, induced apoptosis in C6.9 glioma cells, as determined by DNA fragmentation and loss of plasma membrane asymmetry. THC stimulated sphingomyelin hydrolysis in C6.9 glioma cells. THC and N ‐acetylsphingosine, a cell‐permeable ceramide analog, induced apoptosis in several transformed neural cells but not in primary astrocytes or neurons. Although glioma C6.9 cells expressed the CB1 cannabinoid receptor, neither THC‐induced apoptosis nor THC‐induced sphingomyelin breakdown were prevented by SR141716, a specific antagonist of that receptor. Results thus show that THC‐induced apoptosis in glioma C6.9 cells may rely on a CB1 receptor‐independent stimulation of sphingomyelin breakdown.