Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB196

Poster Communications

Aspirin working with platelet for its anti-cancer role on metastatic breast cancer

Z. Zhang1, F. Chen1, L. Shang1,2

1. Faculty of Life Science, Northwest Univeristy, Xi'an, China. 2. Faculty of Life Sciences, University of Bradford, Bradford, United Kingdom.


Aspirin has recently been considered as potential treatment against cancer. Some studies showed that aspirin has great effect in the primary prevention, secondary prevention of cancer (especially in colorectal cancer etc.) [1, 2] but the specific molecular mechanism is still unknown, particularly its interactive role with platelet in treating cancer. Breast cancer is a malignant disease with extremely high morbidity and mortality. One study [3] summarized the literature on the relationship between breast cancer and aspirin from 2000 to 2012 and indicated aspirin has a preventive effect for breast cancer when the dose exceeds 100 mg/d and the drug is regularly used for more than 3 years or longer. In addition, another study [4] showed that thrombocytosis is positively associated with tumour incidence. In this study, we investigated effects of aspirin against metastatic breast cancer. We used human breast cancer cells 231 and mouse breast cancer cells 4T1 cell lines to test its anti-cancer effects along with human platelet-rich plasma and mouse platelet-rich plasma by proliferation assay, scratch test in vitro. We then used Babl/c mouse inoculated tumors subcutaneously to test the survival period of mice, tumor size, and some physiological and biochemical indicators in vivo. Our results showed that aspirin has an inhibitory effect on the proliferation of tumor cells in vitro. Elevated concentrations of platelet-rich plasma could significantly inhibit cell proliferation after a long time; possibly due to the fibrinogen-formed film prevents tumor cells contact the external environment. Low concentrations of platelet-rich plasma had no effect on tumor cell proliferation. Platelet-rich plasma can advance the invasion of metastatic breast cancer cells, and this effect could be inhibited by aspirin. In vivo results showed that aspirin can significantly prolong the survival time of tumor-bearing mouse, and mouse inoculated with tumor cells co-cultured with platelet-rich plasma in vitro have a higher hazard ratio. Tumor HE staining showed that mouse in the aspirin group had less metastasis cancer cells during the same period, suggesting that platelets play a catalytic role in tumor metastasis and this effect can be inhibited by aspirin. In addition, in the aspirin group the mouse tumor tissue mass exterior was better without wear and ulceration, suggesting that aspirin can reduce the pain in the late stage of cancer and extend the survival time. Biochemical indicators indicated that there is no significant relationship between platelet index and the degree of cancer deterioration, which may be due to the small sample size. In conclusion, our results indicated that the ability of aspirin against clinically advanced breast cancer is relatively limited, and that aspirin, platelets, and tumors may interact with each other through specific pathways, which need further verification.

Where applicable, experiments conform with Society ethical requirements