Investigating the effect of Ibuprofen on DLL1 gene expression in gastric cancer stem cells derived from MKN-45 cell line

Cancer stem cells have ability to self-renewal that it is dominant property for them, also these cells can differentiate to varied tissues [1]. In normal tissues, their ability to self-renewal has been controlled and there is balance between new cells and the differentiated cells. But if the regulation of the stem cell signaling pathways including the Notch signaling pathway disrupted, the proliferation of these cells increases, leading to tumorigenesis [2]. In light of this understanding, targeting the cancer stem cells could reduce the production of new cells. Ibuprofen is one of the nonsteroidal anti-inflammatory drugs (NSAIDs) that can relief pain and control inflammation [3]. Recent studies provide evidence that NSAIDs inhibit the promotion and proliferation of some tumors. In this regard, we can use them for treatment of cancer by focusing on the genes involved in the disease. However, pivotal role of some genes involved in carcinogens have been remain unknown. In this study, we had investigated changes in the expression of DLL1 involved in Notch signaling pathway by qRT-PCR in MKN-45 cell line derived from gastric cancer stem cells in response to ibuprofen. Our results showed that ibuprofen inhibits the proliferation of gastric cancer stem cells by up-regulating DLL1. These findings confirm that this gene acts as tumor-suppressor. Our findings suggest that ibuprofen may be used as an adjuvant chemotherapy drug to improve gastric cancer treatment outcomes.

Keywords:

Gastric cancer(GC) , Ibuprofen , Nonsteroidal anti-inflammatory drugs (NSAIDs).