Effect of aspirin on cancer metastases

The spread of metastases from main tumors to more distant organs leads to death in 90% of cancer cases. Since the 2010s, studies have shown that low-dose aspirin reduces the risk of metastatic spread. The underlying mechanism has only recently been elucidated.

𝐌𝐞𝐭𝐚𝐬𝐭𝐚𝐭𝐢𝐜 𝐜𝐞𝐥𝐥𝐬 are vulnerable to immune attacks because they are not in contact with the tumor's immunosuppressive microenvironment. This vulnerability is a 𝐩𝐨𝐭𝐞𝐧𝐭𝐢𝐚𝐥 𝐭𝐚𝐫𝐠𝐞𝐭 for 𝐩𝐫𝐞𝐯𝐞𝐧𝐭𝐢𝐧𝐠 𝐜𝐚𝐧𝐜𝐞𝐫 𝐩𝐫𝐨𝐠𝐫𝐞𝐬𝐬𝐢𝐨𝐧. The authors of an article recently published in 𝑁𝑎𝑡𝑢𝑟𝑒 described the precise 𝐦𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐦 𝐨𝐟 𝐚𝐜𝐭𝐢𝐨𝐧 of these treatments, while searching for genetic factors regulating metastasis in mice.

𝐓𝐡𝐫𝐨𝐦𝐛𝐨𝐱𝐚𝐧𝐞 𝐀𝟐 (TXA2), a molecule released by platelets, is thought to activate the 𝐴𝑟ℎ𝑔𝑒𝑓1 gene present in 𝐓 𝐥𝐲𝐦𝐩𝐡𝐨𝐜𝐲𝐭𝐞𝐬, which has a “𝐬𝐭𝐚𝐧𝐝𝐛𝐲” effect on these cells. The purpose of these immune cells, also known as white blood cells, is to eradicate abnormal cells. Given that 𝐚𝐬𝐩𝐢𝐫𝐢𝐧 𝐢𝐧𝐡𝐢𝐛𝐢𝐭𝐬 𝐭𝐡𝐞 𝐜𝐲𝐜𝐥𝐨𝐨𝐱𝐲𝐠𝐞𝐧𝐚𝐬𝐞 𝟏 𝐞𝐧𝐳𝐲𝐦𝐞, which is essential for TXA2 production, this explains aspirin's effect on the 𝐦𝐞𝐭𝐚𝐬𝐭𝐚𝐬𝐢𝐬 𝐩𝐫𝐨𝐥𝐢𝐟𝐞𝐫𝐚𝐭𝐢𝐨𝐧 through T-cell activation.

Given that not all cancers trigger exactly the same type of 𝐫𝐞𝐚𝐜𝐭𝐢𝐨𝐧 𝐚𝐭 𝐦𝐨𝐥𝐞𝐜𝐮𝐥𝐚𝐫 𝐥𝐞𝐯𝐞𝐥, aspirin would be effective against 𝐚𝐝𝐞𝐧𝐨𝐜𝐚𝐫𝐜𝐢𝐧𝐨𝐦𝐚𝐬 (colorectal, gastric, breast and lung cancers), but its efficacy would be diminished against other types of cancer. This discovery is a 𝐯𝐞𝐫𝐲 𝐞𝐧𝐜𝐨𝐮𝐫𝐚𝐠𝐢𝐧𝐠 𝐥𝐞𝐚𝐝 for hindering metastatic dissemination.