Aspirin may help slow the growth of localized colon and pancreatic cancers by inhibiting the cross-talk between cancer cells and platelets, according to research published in the American Journal of Physiology – Cell Physiology.
The study, “Aspirin therapy reduces the ability of platelets to promote colon and pancreatic cancer cell proliferation: implications for the oncoprotein c-MYC,” sheds new light on how the anti-inflammatory drug reduces the risk of some cancers, including colon cancer.
Aspirin (acetylsalicylic acid) has been the subject of intensive investigation for more than a century due to its anti-inflammatory and anti-platelet properties. In addition to its cardioprotective effects, aspirin has also been associated with reduced risk of cancer. But until now, researchers didn’t understand how aspirin exerted its anti-cancer effects.
Researchers at Oregon Health and Science University and Oregon State University focused their research on how aspirin modified platelet pro-tumoral properties.
They had a hunch that aspirin’s anti-cancer properties could be linked to platelets because low, anti-platelet doses of aspirin were more effective in decreasing colorectal cancer incidence and mortality than high, anti-inflammatory doses.
Consistent with such findings, platelets have been shown to play a key role in promoting tumor survival, growth, and metastasis through the release of pro-tumor growth factors.
Such results were confirmed by the team when they placed platelets on top of metastatic and non-metastatic colon cancer cells (isolated from the different regions of the same patient) and pancreatic cancer cells.
But, confirming the team’s suspicions, when aspirin was added to the culture, the platelets no longer exerted their pro-tumor effects on the non-metastatic colon cancer and pancreatic cancer cells. The metastatic colon cancer cells, however, continued to grow after low-dose aspirin treatment and only very high doses — that cannot be taken orally — were effective in stopping the growth of such cells.
The researchers also found that the platelet pro-tumoral effect was dependent on the activation of the pro-tumoral protein c-Myc within cancer cells. The c-Myc protein is a transcription factor that controls nearly 15 percent of all human genes, including genes involved in cell cycle, survival, protein synthesis, and cell metabolism. Not surprisingly, high levels of c-Myc are found in a number of cancers, including colon, pancreas, breast, lung, and prostate cancers.
The researchers found that metastatic colon cancer cells already had high levels of c-Myc protein at baseline, which was likely why aspirin did not slow the proliferation of the metastatic cells.
Together, the findings suggest that platelet interaction with cancer cells is a key mechanism involved in tumor growth and spread, and that low-dose aspirin treatment may slow the growth of non-metastatic cells by preventing the platelet-induced activation of c-Myc in cancer cells.
“We propose a novel anti-cancer mechanism of action of low-dose aspirin, namely through the inhibition of platelet-induced molecular signals that cause aberrant expression of c-MYC oncoprotein in non-metastatic cancers,” the researchers wrote.
“Because the interaction between platelets and cancer cells is believed to occur early following intravasation, the use of anti-platelet doses of aspirin might serve as a safe and efficacious preventive measure for patients at risk for cancer,” they added.
