The active ingredient in Viagra, sildenafil, may play a role in preventing cancer from spreading by restricting cancer cells' access to cholesterol, according to a new study published by the American Association for Cancer Research. The research, conducted by scientists at the Weizmann Institute of Science in Israel and including collaborators at the U.S. National Cancer Institute, investigated the potential anti-cancer properties of sildenafil, a PDE5 inhibitor commonly known as Viagra.
Researchers analyzed data from human and mouse cancer cells, alongside 20 years of health records from over five million individuals in Israel. Their findings indicate that sildenafil limits cancer cells' capacity to utilize cholesterol, a process essential for tumor cells to detach from a primary tumor and migrate throughout the body. Cholesterol is vital for cancer cells to break away from the main tumor and spread.
Sildenafil works by inhibiting the enzyme phosphodiesterase type 5 (PDE5) and increasing cyclic guanosine monophosphate (cGMP). While this mechanism contributes to Viagra's effectiveness in treating erectile dysfunction by dilating blood vessels, the study suggests it also impacts cancer cells. The increased cGMP binds to a protein that transports cholesterol within cells, thereby reducing the cholesterol available for cellular functions. Cancer cells, which are particularly reliant on cholesterol, appear to be vulnerable to this reduction.
The study’s authors proposed that combining sildenafil-based medications with statins, drugs that lower cholesterol, could potentially enhance the inhibition of cancer spread. By reducing cholesterol production and limiting cancer cells' access to it, this combination might slow tumor metastasis. Professor Ayelet Erez, a senior researcher involved in the study, noted that the findings highlight how a patient's metabolic state and existing medications can influence cancer biology, underscoring the importance of a holistic approach to cancer treatment.
The researchers acknowledge that the study's reliance on mouse models presents a limitation, as findings may not always directly translate to human patients. Furthermore, the human data is observational, indicating an association rather than a definitive cause-and-effect relationship. Dr. Loren Rourke, a breast cancer surgeon, author, and speaker, has previously confirmed research suggesting that glucagon-like peptide-1 medications might be linked to a lower risk of cancer recurrence and new diagnoses, indicating a broader interest in how existing medications could impact cancer outcomes.