Epigenetic Regulation by Androgen Receptor in Prostate Cancer

Takayama, Ken‐ichi

doi:10.21926/obm.genet.1804047

Cited by 3 publications

(3 citation statements)

References 126 publications

(225 reference statements)

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“…Several studies now suggest that also the AR is implicated in shaping the chromatin structure by modifying the activity of epigenetic factors (Takayama 2018). Through transcriptomic profiling of isogenic AR-overexpressing CRPC cell line models ('mimicking' adenocarcinoma-CRPC) and LuCaP PDXs with different AR expression levels (Urbanucci et al 2008, 2012a,b, 2013Waltering et al 2009, Jalava et al 2012, it was shown that high AR levels associated with increased expression of androgen-responsive genes and AR coregulators.…”

Section: The Androgen Receptor Drives Chromatin Relaxation As An Oncomentioning

confidence: 99%

Chromatin reprogramming as an adaptation mechanism in advanced prostate cancer

Braadland

Urbanucci

2019

Endocrine-Related Cancer

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Tumor evolution is based on the ability to constantly mutate and activate different pathways under the selective pressure of targeted therapies. Epigenetic alterations including those of the chromatin structure are associated with tumor initiation, progression and drug resistance. Many cancers, including prostate cancer, present enlarged nuclei, and chromatin appears altered and irregular. These phenotypic changes are likely to result from epigenetic dysregulation. High-throughput sequencing applied to bulk samples and now to single cells has made it possible to study these processes in unprecedented detail. It is therefore timely to review the impact of chromatin relaxation and increased DNA accessibility on prostate cancer growth and drug resistance, and their effects on gene expression. In particular, we focus on the contribution of chromatinassociated proteins such as the bromodomain-containing proteins to chromatin relaxation. We discuss the consequence of this for androgen receptor transcriptional activity and briefly summarize wider gain-of-function effects on other oncogenic transcription factors and implications for more effective prostate cancer treatment.

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Section: The Androgen Receptor Drives Chromatin Relaxation As An Oncomentioning

confidence: 99%

Chromatin reprogramming as an adaptation mechanism in advanced prostate cancer

Braadland

Urbanucci

2019

Endocrine-Related Cancer

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“…Once keloid is formed, it is harder to cure, and it has a high recurrence rate no matter how it is treated [30]. Although the outcomes of keloid are not as severe as those of various cancers, such as neurodegenerative diseases and cardiovascular diseases, they similarly affect people's normal lives [31][32][33]. CircRNAs are recently discovered potential gene therapeutic targets in a range of diseases.…”

Section: Discussionmentioning

confidence: 99%

Circ_0008450 downregulates Runx3 to promote the proliferation and epithelial-mesenchymal transition of human keratinized epithelial cells

Chen

Xu²,

Lai

et al. 2020

Cell Cycle

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Keloid is an extremely common and often overlooked benign neoplastic disease, but its consequences should not be underestimated. Therefore, a deep exploration of the pathological mechanism of keloid becomes very essential. After 22 samples were collected from each patient's keloid tissues and normal skin tissues, circ_0008450 and Runx3 expression was tested by qRT-PCR. When primary human keratinized epithelial cells were transfected by sh-circ_0008450 or sh-Runx3, cell proliferation, apoptosis, migration, and EMT process were assessed by CCK-8, BrdU assay, apoptosis assay, migration assay, and Western blot. Finally, transfection was performed to explore the effect of circ_0008450 on the TGF-β/Smad signal pathway by adopting western blot. Circ_0008450 was highly expressed in keratinized epithelial tissues. After the transfection of sh-circ_0008450 into primary human keratinized epithelial cells, cell proliferation, migration, and EMT process were inhibited, and apoptosis was stimulated. Moreover, circ_0008450 silence-induced above changes were partly reversed by transfecting sh-Runx3. In addition, transfecting sh-circ _0008450 could repress TGF-β/Smad pathway, while transfecting sh-Runx3 activated the above pathway. Circ_0008450 down-regulated Runx3 to promote the proliferation and EMT process of human keratinized epithelial cells. This discovery may be related to the activation of the TGF-β/ Smad pathway.

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“…Several studies now suggest that also the AR is implicated in shaping the chromatin structure by modifying the activity of epigenetic factors (Takayama. 2018).…”

Section: The Androgen Receptor Drives Chromatin Relaxation As An Oncomentioning

confidence: 99%

Chromatin reprogramming as adaptation mechanism in advanced prostate cancer

Urbanucci¹

2018

European Urology Supplements

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Tumor evolution is based on the ability to constantly mutate and activate different pathways under the selective pressure of targeted therapies. Epigenetic alterations including those of the chromatin structure are associated with tumor initiation, progression, and drug resistance. Many cancers, including prostate cancer, present enlarged nuclei and chromatin appears altered and irregular. These phenotypic changes are likely to result from epigenetic dysregulation. High-throughput sequencing applied to bulk samples and now to single cells has made it possible to study these processes in unprecedented detail. It is therefore timely to review the impact of chromatin relaxation and increased DNA accessibility on prostate cancer growth and drug resistance, and their effects on gene expression. In particular, we focus on the contribution of chromatinassociated proteins such as the bromodomain-containing proteins to chromatin relaxation. We discuss the consequence of this for androgen receptor transcriptional activity and briefly summarize wider gain-offunction effects on other oncogenic transcription factors and implications for more effective prostate cancer treatment.

show abstract

Epigenetic Regulation by Androgen Receptor in Prostate Cancer

Cited by 3 publications

References 126 publications

Chromatin reprogramming as an adaptation mechanism in advanced prostate cancer

Chromatin reprogramming as an adaptation mechanism in advanced prostate cancer

Circ_0008450 downregulates Runx3 to promote the proliferation and epithelial-mesenchymal transition of human keratinized epithelial cells

Chromatin reprogramming as adaptation mechanism in advanced prostate cancer

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