Aspirin Attenuates Tumor Initiating Cell Growth And Induces Reprogramming Factors Of Mesenchymal To Epithelial Transition In Breast Cancer Cell

Acetyl Salicylic Acid (ASA) also known as aspirin, a classic, non-steroidal, anti-inflammatory drug (NSAIDs) is widely used to relieve minor aches and pains and to reduce fever. Epidemiological studies and other experimental studies suggest that ASA use reduces the risk of different cancers including breast cancer (BC) and may be used as a chemo-preventive agent against BC and other cancers. These studies have raised the tempting possibility that ASA could serve as a preventive medicine for BC. However, lack of in-depth knowledge of the mechanism of action of ASA reshapes the debate of risk and benefit of using ASA in prevention. Our studies, using in vitro and in vivo tumor xenograft model, show a strong beneficial effect of ASA in the prevention of breast carcinogenesis. We find ASA not only prevents breast tumor cell growth in vitro and tumor growth in nude mice xenograft model through the induction of apoptosis, it also significantly reduces the growth of tumor initiating cells (TICs)/ cancer stem cells (CSCs) and delayed the formation of a palpable tumor. Moreover, ASA regulates other pathophysiological events in breast carcinogenesis, such as reprogramming the mesenchymal to epithelial transition (MET) and delaying in vitro migration in BC cells. The tumor growth-inhibitory as well as reprogramming roles of ASA could be mediated through inhibition of TGF-β-signaling pathway, which is associated with growth, motility, invasion and metastasis in advanced breast cancers. Collectively, ASA has a therapeutic or preventive potential by attacking possible target such as TGF-β- SMAD4 signaling in breast carcinogenesis. [This work is funded by VA Merit Awarded Grant (SB and SKB)] Note: This abstract was not presented at the meeting. Citation Format: Gargi Maity, Archana De, Snigdha Banerjee, Amlan Das, Sandipto Sarkar, Sushanta K. Banerjee. Aspirin attenuates tumor initiating cell growth and induces reprogramming factors of mesenchymal to epithelial transition in breast cancer cell. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5410. doi:10.1158/1538-7445.AM2015-5410