Abstract

Abstract Inflammation is implicated in prostate cancer initiation and progression. Our lab found that the inflammatory cytokine, interleukin-1 beta (IL-1β) concomitantly upregulates the pro-survival scaffold protein, Sequestome-1 (SQSTM1/p62) and represses androgen receptor accumulation in a relatively small cell subpopulation within various prostate cancer cell lines. Given that cancer stem cell subpopulations have been isolated from isogenic cell lines and given that prostate cancer stem cells are androgen receptor negative, we hypothesized that the IL-1β-responsive subpopulation might be stem-like cells. Cancer stem cells are significant in prostate cancer because they are resistant to chemo-radiation and androgen-targeted therapies and can contribute to the tumor cell pool through asymmetric division. Thus, we analyzed the mRNA and protein accumulation of several stem cell markers in various prostate cancer cells lines exposed to IL-1β. We also have experiments underway to analyze stem cell biology in order to determine the functional significance of the IL-1β-responsive subpopulation. Thus far, we have discovered that IL-1β can induce stem cell marker mRNA and protein accumulation, suggesting that IL-1β alters prostate cell fate and supports the notion that inflammation contributes to prostate cancer initiation and progression. Citation Format: Shayna Thomas, Sana Merchant, Rachel Meade, Afshan Fathima Nawas, Nikki Delk. Interlukin-1 (IL-1) may induce prostate cancer (PCa) stem-like cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2533.

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