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Abstract
Cancer cells, especially cancer stem cells (CSCs), are known for their therapeutic resistance and ability to induce a cancer relapse even many years after successful treatment. The quest for a novel protocol utilizing some commonly used non-oncologic drugs that would improve patients outcomes seems to be the right solution. Aspirin (ASA) is one of such eminent drugs. Our study demonstrated that ASA may exert synergistic effect with the anti-Fas antibody on CSCs of colorectal cancer cell lines. We found that such compound treatment inhibited the pro-cancerous effect of anti-Fas stimulation and decreased spherogenicity, survival and CD133-positive cells’ count. Additionally, ASA with anti-Fas antibody may have a positive impact on dendritic cells’ functions. Our innovative study explored simultaneous usage of two biologically active compounds which haven’t been considered in such combination to assess their significance in colorectal cancer cell biology.
Highlights
Colorectal cancer (CRC), one of the most serious health issues globally, ranks third in incidence and second in mortality among cancers worldwide
HT29 cells origin from rectosigmoid part of intestine, whereas HCT116 is adenocarcinoma cells line, for simplicity of our manuscript, the cells analyzed from both cell lines we defined as colorectal cancer stem cells
Cancer cells of two human CRC lines were treated with the combination of anti-Fas agonistic antibody (200 ng/mL) and 2.2 mM and 1.8 mM ASA for HCT116 and HT29 cell lines, respectively
Summary
Colorectal cancer (CRC), one of the most serious health issues globally, ranks third in incidence and second in mortality among cancers worldwide. Chemotherapy, a baseline treatment for colorectal cancer, should be limited in the clinics due to the high resistance of cancer cells and the number of side effects. The study evaluating some novel combinations of active agents can point the appealing and tempting pathways for future clinical efforts. The regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is believed to trigger a prominent anticancer effect, as the increased level of prostaglandins within CRC tissue was detected [2,3]. The comprehensive meta-analysis by Bosetti et al, supported earlier conclusions and confirmed an inverse association between regular ASA use and the risk of CRC and other digestive tract cancers [4]. ASA’s anti-tumor activity is believed to be based on a selective induction of apoptosis in cancer cells [5,6]. The mechanism underlying its pro-apoptotic activity is complex and remains elusive
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