New research shows that CBD may suppress metastasis in pancreatic cancer by disrupting molecular drivers of tumor cell invasion.
A study published in IUBMB Life and conducted by researchers at Kyung Hee University has found that cannabidiol (CBD), a non-psychoactive compound derived from marijuana, may inhibit the spread of pancreatic ductal adenocarcinoma (PDAC) by targeting key pro-metastatic pathways.
Using three pancreatic cancer cell lines, the study demonstrated that CBD suppresses the expression of chemokine receptors CXCR4 and CXCR7, as well as the matrix metalloproteinases MMP-2 and MMP-9—proteins known to facilitate cancer cell invasion. CBD also reversed changes typically associated with epithelial–mesenchymal transition (EMT), a biological process closely tied to metastasis and chemoresistance. Treatment led to increased expression of epithelial markers like E-cadherin and Occludin, while decreasing mesenchymal markers such as Snail and Vimentin.
Central to these effects is MALAT1, a long non-coding RNA highly expressed in pancreatic tumors. CBD treatment downregulated MALAT1, which the researchers found to be a major upstream regulator of both EMT and the PI3K/Akt/mTOR pathway—a signaling cascade that promotes tumor growth, invasion, and resistance to therapy. Overexpressing MALAT1 in cancer cells triggered EMT and increased activity in the PI3K/Akt/mTOR axis, but CBD was able to reverse these changes.
Importantly, when CBD was combined with low-dose gemcitabine—a common chemotherapy drug for PDAC—it produced a synergistic effect, enhancing suppression of EMT markers, MALAT1 expression, and related signaling pathways without causing significant toxicity. This suggests a potential role for CBD as a chemosensitizer in pancreatic cancer treatment.
While the results are promising, the study was limited to in vitro models and did not include in vivo or human clinical trials. Nonetheless, the findings offer new insight into how CBD may interfere with metastasis at the molecular level, and support its continued evaluation as a therapeutic partner in PDAC management.
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