Recent medical research has highlighted a major problem with cancer: cancer cells display plasticity. Some cancer cells can spontaneously revert from a differentiated state to become immature and stem-cell-like again, yielding more diverse, aggressive and fast-growing tumors. This makes them thwart traditional treatments such as chemotherapy and radiation, which aim to stop cellular division and kill cancer cells outright.
THC “Locks In” Cancer
In a new experiment, researchers used the cannabis compound THC to push cancer cells to “lock in” and make tumors less aggressive. In a study published in Communications Biology, researchers explored the effects of an ultra-low-dose, 4-day cannabinoid treatment on organoids — lab-built 3D breast-tumor models made from breast cancer cells — as well as in mouse models.
The CB2R Receptor Is Key
The treatment targeted the endocannabinoid system, which can regulate developmental pathways paralleled in both cancer evolution and embryonic development. After a 4-day low-dose pulse of THC (an agonist), the organoids showed reduced invasiveness, self-renewal capacity and tumor initiation. The result appears to be mediated mainly by the CB2R receptor, linked to inflammatory responses, rather than CB1R, linked to cannabis’ psychoactive effects.
The “Good Cop Bad Cop” Routine
The researchers used a biomolecular “good cop bad cop” strategy. They treated CB1R and CB2R with separate inverse agonists (SR1 and SR2, respectively) that reduce the receptors’ baseline activity. Despite this, the organoids became less cancer-cell-like. Surprisingly, the CB2R inverse agonist SR2 reproduced THC’s tumor-inhibiting effects, while the CB1R agonist SR1 did not. But organoids from mice lacking CB2R showed similar changes — suggesting the receptor’s baseline activity itself is important.
Effects Persist In Vivo
The effects proved stable in vivo. Tumor-inhibiting effects persisted for up to 100 days when THC-treated organoids were transplanted into living cancer-prone mice, which developed tumors later and showed slower tumor growth. In a separate experiment, THC-treated cells produced fewer clusters in the lungs four weeks after injection.
Avenues for Treatment
The researchers also found that CB2R modulation appears to increase estrogen receptor activity, making breast cancer cells more responsive to endocrine therapy with the common drug tamoxifen. The research opens avenues to control the process and influence cancer cell behavior with subtle CB2R modulation, with effects persisting long after cannabinoid withdrawal.
“This view is consistent with the concept that tumor cell populations occupy continuous and dynamic state landscapes, where relatively small perturbations can trigger large-scale and self-reinforcing transitions in collective behavior,” the researchers conclude.
Source:
Scientists Discover a Cannabis Receptor That Could Stop Breast Cancer Spreading — ScienceAlert
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