Apr 23, 2020

Chronic IL-1 exposure drives LNCaP cells to evolve androgen and AR independence

BioRxiv : the Preprint Server for Biology
H. DahlNikki Delk

Abstract

Background: Chronic inflammation is a known cause of prostate cancer (PCa) initiation and progression. Interleukin-1 (IL-1) is an inflammatory cytokine secreted by tumor cells and bone-derived immune cells that contributes to chronic inflammation in the tumor microenvironment. IL-1 is elevated in PCa patients and contributes to PCa progression and treatment resistance. IL-1 has been shown to promote PCa metastasis and bone colonization, shown to recruit mesenchymal stems cells to the tumor to support castration-resistant PCa (CRPCa) development and chronic IL-1 exposure was shown to promote PCa anti-androgen resistance. We previously reported that acute IL-1 exposure represses androgen receptor (AR) accumulation and activity, providing a possible mechanism for IL-1-mediated development of androgen- and AR-independent PCa. Given that acute inflammation is quickly resolved, and chronic inflammation is, instead, co-opted by cancer cells to promote tumorigenicity, we set out to determine if chronic IL-1 exposure leads to similar repression of AR and AR activity observed for acute IL-1 exposure and to determine if chronic IL-1 exposure selects for androgen- and AR-independent PCa cells. Methods: We isolated isogenic LNCaP sublines f...Continue Reading

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Mentioned in this Paper

Crystal - Body Material
Protein Binding
Protein Biotinylation
Carbon
Embedding
Electron Microscopy, Diagnostic
Macromolecule
Electron Microscopy
Ribosomes
Biotin

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