الفهرس | Only 14 pages are availabe for public view |
Abstract Tumor associated macrophages (TAMs) provide the tumor microenvironment with multiple inflammatory mediators to stimulate several intrinsic pathways, consequently they have a crucial role in cancer progression and metastasis and therapeutic response. Although the role of non steroidal anti-inflammatory drugs (NSAIDs) in prevention of cancer incidence and progression has been documented in several types of cancer, its role in suppression the interactions between TAMs and cancer cells remain unclear. The aim of the present study was to determine the contribution of secretions of TAMs to breast cancer progression through intrinsic events, such as modulation of Ras and Par-4 expression, and stimulation of inflammatory mediators production such as IL-1Ý, IL-6, Cox-2 and PGE2 which found to be highly expressed in more than 40% of breast cancer patients. Furthermore, we examined the mechanism by which NSAIDs (sulindac sulfide and piroxicam) suppress the progression of stimulated breast cancer cells. In present study media conditioned by U937 human monocytes (U937-CM) were used to stimulate MCF-7 and MDA-MB-231 human breast cancer cells, we determined the tumor promoting activity of U937-CM on MCF-7 and MDA-MB-231 cells |