According to a study, Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo.
The primary cannabinoid of marijuana, Δ9-Tetrahydrocannabinol (THC), has been shown to either inhibit or potentiate tumor growth, depending on the cancer type and its pathogenesis. Little is known about activity of cannabinoids such as THC on epidermal growth factor receptor-over expressing lung cancers that are often highly aggressive and resistant to chemotherapy.
In the study, the researchers characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell lung cancer using the cell lines A549 and SW-1573 as in vitro models. It was found that these cells express cannabinoid receptors CB1 and CB2, known targets for THC action. It was also found that THC inhibited EGF-induced growth, chemotaxis, and chemoinvasion. The signaling studies indicated that THC could act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT. The primary cannabinoid of marijuana was also responsible for inducing phosphorylation of focal adhesion kinase at tyrosine 397.
Additionally, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls in vivo studies. Tumor samples from animals treated with THC revealed anti-proliferative and anti-angiogenic effects of THC.
The study suggested that cannabinoids such as THC must be explored as novel therapeutic molecules to control the growth and metastasis of certain lung cancers.
Oncogene 10: 339-346