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- W2890148842 abstract "Colorectal cancer (CRC) is one of the major causesof cancer globally. Recent studies proposed a role for cancerinitiating cells (CICs), a small subset of replication-competentcells, in colon carcinogenesis. Although the role of inflammatorylipid-mediators in CRC progression is well known, their role in thepromotion of cancer-initiating cells remains to be elucidated. Forthis thesis, we investigated the role of eicosanoids – leukotrieneD4 (LTD4) or prostaglandin E2 (PGE2) – on CIC properties andchanges occurring in the tumor environment that could possiblysupport CIC-induced tumor growth. To this end, we identified theCICs on the basis of ALDH expression and evaluated their in vitrocharacteristics like colony formation, radio or chemoresistance andin vivo tumorigenic properties in the presence of LTD4 or PGE2. Weshowed that LTD4 and PGE2 enriched the ALDH+ cell population andaugmented the colonies formation and tumor progression in xenograftmice model. The ALDH+ cells were also resistant to 5-fluorouraciland radiation that is additionally augmented by both thelipid-mediators. Moreover the impact of lipid inflammatorymediators on the stemness properties of CICs was evident byincreased expression of genes that confer survival and self-renewalability to CICs. In immunodeficient mice, LTD4 or PGE2 treatmentamplified CIC-induced tumor growth. Furthermore, LTD4 and PGE2increased cell proliferation activated β-catenin signaling andup-regulated COX-2. Additionally, LTD4 or PGE2 drive massiveinflammatory responses identified as CD45+ enrichment, particularlyof macrophages within tumors. The ability of ALDH+ cells to formtumors in immunodeficient mice could not be challenged by radiationtherapy. In a separate series of experiments, we investigated thecontribution of CICs in the development of sensitivity againstmontelukast, a CysLT1R antagonist. In this context we report thatsensitivity of tumors against montelukast could depend on thevariation in CICs content, activation of prosurvival factors suchas BCL-2 and β-catenin signaling. Collectively, our data showedthat LTD4 and PGE2 exacerbate CIC characteristics and promote tumorgrowth by allowing modifications in the tumor environment. Newtherapeutic strategies could aim to resolve not only cancerassociated inflammation, but also to target CICs in order toachieve better remission and cure advanced colon cancerstages." @default.
- W2890148842 created "2018-09-27" @default.
- W2890148842 creator A5012668295 @default.
- W2890148842 date "2015-01-01" @default.
- W2890148842 modified "2023-09-24" @default.
- W2890148842 title "The Role of Inflammatory Lipid Mediators on Colon CancerInitiating Cells (CICs)" @default.
- W2890148842 hasPublicationYear "2015" @default.
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