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IL-1β expression driven by androgen receptor absence or inactivation promotes prostate cancer bone metastasis
Journal article   Open access   Peer reviewed

IL-1β expression driven by androgen receptor absence or inactivation promotes prostate cancer bone metastasis

Anthony DiNatale, Asurayya Worrede, Waleed Iqbal, Michael Marchioli, Allison Toth, Martin Sjöström, Xiaolin Zhu, Eva Corey, Felix Y. Feng, Wanding Zhou, …
Cancer research communications, v 2(12), pp 1545-1557
01 Dec 2022
PMID: 36561929
url
https://aacrjournals.org/cancerrescommun/article-pdf/2/12/1545/3228553/crc-22-0262.pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1158/2767-9764.crc-22-0262View
Published, Version of Record (VoR) Open

Abstract

Androgen Receptor IL-1β Metastasis Methylation Prostate Cancer
We report the inverse association between the expression of androgen receptor (AR) and interleukin-1beta (IL-1β) in a cohort of patients with metastatic castration resistant prostate cancer (mCRPC). We also discovered that AR represses the IL-1β gene by binding an androgen response element (ARE) half-site located within the promoter, which explains the IL-1β expression in AR-negative (AR NEG ) cancer cells. Consistently, androgen-depletion or AR-pathway inhibitors (ARIs) de-repressed IL-1β in AR POS cancer cells, both in vitro and in vivo . The AR transcriptional repression is sustained by histone de-acetylation at the H3K27 mark in the IL-1β promoter. Notably, patients’ data suggest that DNA methylation prevents IL-1β expression, even if the AR-signaling axis is inactive. Our previous studies show that secreted IL-1β supports metastatic progression in mice by altering the transcriptome of tumor-associated bone stroma. Thus, in prostate cancer patients harboring AR NEG tumor cells or treated with ADT/ARIs, and with the IL-1β gene unmethylated, IL-1β could condition the metastatic microenvironment to sustain disease progression.

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Web of Science research areas
Oncology
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