Aspirin may hinder proliferation of some colon and pancreatic cancers

Aspirin—common salicylic acid found in the bark of willow trees and used as a pain and fever reducer for 2000 years—may slow the spread of some colon and pancreatic cancer cells, according to a recent study published in the American Journal of Physiology—Cell Physiology.

Researchers had previously found that low doses of aspirin may reduce the risk of some gastrointestinal cancers, possibly because it is an anti-platelet drug. Platelets have been implicated in every phase of cancer cell growth, which they may promote via the release of growth factors, such as TGFß, that may heighten the response of oncoproteins, which are known to regulate tumor cell development. Activated platelets may also play a role in metastasis by protecting circulating tumor cells from the body’s immune response.

Based on these and other previous findings, researchers focused on the anti-platelet properties of aspirin.

“The current study aimed to determine the effect of aspirin on the crosstalk between platelets and cancer cells. Our results suggest that low-dose aspirin might be efficacious in reducing the proliferation of cancer cells through the inhibition of platelet-derived signals required for the upregulation of the oncoprotein c-MYC,” wrote these authors, led by Annachiara Mitrugno, of Oregon Health and Science University, Portland, OR.

Mitrugno and coworkers combined activated platelets primed for clotting process with three types of cancer cells: metastatic colon cancer, nonmetastatic colon cancer, and nonmetastatic pancreatic cancer. Researchers used two colon cancer cell lines from the same donor, characterized by different metastatic potential, SW480 (nonmetastatic) and SW620 (metastatic) cancer cells, and a pancreatic cancer cell line, PANC-1 (nonmetastatic).

Aspirin was added to the mixture, and in response, platelets in the pancreatic and nonmetastatic colon cancer cells couldn’t stimulate growth and replication, although growth continued in metastatic colon cancer cells. Only very high doses of aspirin could stop the growth in these cells.

In addition, low doses of aspirin in pancreatic cancer cells stopped the release of growth factor from platelets and reduced oncoprotein signaling.

“Our study reveals important differences and specificities in the mechanism of action of high- and low-dose aspirin in metastatic and nonmetastatic cancer cells with different tumor origins and suggests that the ability of aspirin to prevent platelet-induced c-MYC [an oncoprotein] expression might be selective for a nonmetastatic phenotype,” these authors concluded.