Study Finds Cannabinoids May Increase Lung Cancer’s Susceptibility to Specialized Killer Cells
Results from a recent study suggest that cannabinoids indirectly make cancer cells more susceptible to being broken down by cells programmed to kill tumors.
Supporters of medical cannabis have often suggested that cannabis offers a significantly milder form of cancer treatment compared to traditional approaches, such as chemotherapy. These claims have been supported by a growing body of evidence that cannabis can inhibit the spread of cancer, as well as cause cancerous cell death through a range of diverse mechanisms. A team of researchers from Germany conducted a study to further investigate the interaction between cannabis and lung cancer.
Cannabinoids have been found to increase the expression of intercellular adhesion molecule 1 (ICAM-1) as part of the mechanism in fighting the invasiveness and spread of lung cancer cells. The team, led by Maria Haustein, PhD, investigated the impact of this cannabinoid-induced ICAM-1, and published their results in the journal Biochemical Pharmacology.
The researchers were particularly interested in learning how the increased expression of ICAM-1 affected cancer cell adhesion to lymphokine-activated killer (LAK) cells. LAK cells are white blood cells that have been stimulated to fight tumor cells. The research team also investigated how the ICAM-1 impacted LAK cell-mediated cytotoxicity by using in vitro cell culture models.
They found that cannabidiol (CBD) enhanced the susceptibility of cancer cells to adhere to, and be broken down by LAK cells. These effects were reversed when the ICAM-1 was neutralized through several pathways including specific small interfering RNA (siRNA), antagonists to cannabinoid receptors (CB1, CB2), and antagonists to transient receptor potential vanilloid 1 (TRPV1). Additionally, enhanced killing of CBD-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen-1 (LFA-1), suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process. The team determined that tetrahydrocannabinol (THC) sets a similar process in motion that is equally dependent on ICAM-1 for LAK cell-mediated cytotoxicity.
The team concluded, “Altogether, our data demonstrate cannabinoid-induced upregulation of ICAM-1 on lung cancer cells to be responsible for increased cancer cell susceptibility to LAK cell-mediated cytolysis. These findings provide proof for a novel antitumorigenic mechanism of cannabinoids.”
Last updated: 9/2/14; 2:15pm EST