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Cannabidiol (CBD) May Increase Lung Cancer’s Susceptibility To Specialized Killer Cells

Proponents of medical marijuana have long suggested that cannabis offers a much milder form of cancer treatment in comparison to traditional western approaches like chemotherapy.

Supporting these claims is a rapidly growing body of evidence that cannabis can not only inhibit the spread of cancer, but it can cause cancerous cell death through a number of diverse mechanisms.

A team of researchers from Germany published a study last month in the journal Biochemical Pharmacology that sheds further light on the interaction between cannabis and lung cancer in particular. Their results suggest that cannabinoids indirectly make cancer cells more susceptible to being broken down by cells programmed to kill tumors.

German Researchers Investigate THC, CBD, and Lung Cancer

Cannabinoids have been found to increase the expression of the intercellular adhesion molecule 1 (ICAM-1) as part of the mechanism in fighting the invasiveness and spread of lung cancer cells. The team of German researchers, led by Maria Haustein, PhD, set out to test the impact of this cannabinoid-induced ICAM-1.

They were particularly interested in learning how the increased expression of ICAM-1 affected cancer cell adhesion to lymphokine-activated killer (LAK) cells, which are white blood cells that have been stimulated to kill tumor cells.

Cannabidiol (CBD) enhanced the susceptibility of cancer cells to adhere to, and be broken down by LAK cells.”

Utilizing in vitro cell culture models, Haustein’s research team also investigated how the ICAM-1 impacted LAK cell-mediated cytotoxicity.

According to their results, cannabidiol (CBD) enhanced the susceptibility of cancer cells to adhere to, and be broken down by LAK cells. Both of these effects were reversed when the ICAM-1 was neutralized through a variety of pathways including the following: specific small interfering RNA (siRNA), antagonists to cananbinoid receptors (CB1, CB2), and antagonists to transient receptor potential vanilloid 1 (TRPV1).

The enhanced killing of lung cancer cells from CBD treatment was similarly reversed when LAK cells were preincubated with an antibody to lymphocyte function associated antigen-1 (LFA-1) – an adhesion molecule that routinely binds to the ICAM-1. This suggests that the link between the ICAM-1 and LFA-1 is a crucial aspect of CBD-induced cytotoxicity.

Many advocates of medical marijuana hold the belief that tetrahydrocannabinol (THC) is absolutely necessary when treating cancer with cannabis medicine. Sure enough, the German research team determined that THC sets a similar process in motion that is equally dependent on the ICAM-1 for LAK cell-mediated cytotoxicity.

What The Data Points To

In conclusion, Haustein’s research team had the following to say: “our data demonstrate cannabinoid-induced up-regulation of ICAM-1 on lung cancer cells to be responsible for increased cancer cell susceptibility to LAK cell-mediated cytolysis (breaking down of cell). These findings provide proof for a novel antitumorigenic mechanism of cannabinoids.”

It is widely recognized that cannabis has a much milder side-effect profile than that of traditional chemotherapy drugs commonly used to treat cancer. With such distinct proof available for treating various cancers with cannabis medicine, it can only be a matter of time before we start to see a change in federal policy that currently claims cannabis has no medicinal benefits.