Procyanidin B3, an inhibitor of histone acetyltransferase, enhances the action of antagonist for prostate cancer cells via inhibition of p300-dependent acetylation of androgen receptor

Choi, Kyung‐Chul; Park, Si-Yong; Lim, Beom Jin; Seong, Ah-Reum; Lee, Yoo‐Hyun; Shiota, Masaki; Yokomizo, Akira; Naito, Seiji; Na, Younghwa; Yoon, Ho Geun

doi:10.1042/bj20100980

Cited by 54 publications

(26 citation statements)

References 30 publications

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“…Hence, inhibition of aberrant AR signaling is a promising strategy for treating androgendependent prostate cancer as well as CRPC patients (Snoek et al 2009, Tran et al 2009, de Bono et al 2011, Yamashita et al 2012. Therefore, we developed various novel smallmolecule inhibitors that suppress AR expression and function, such as antioxidant N-acetylcysteine (Shiota et al 2012a), methyltransferase inhibitor adenosine dialdehyde (Shiota et al 2012b), HMG-CoA reductase inhibitor statin , protein kinase A inhibitor H89 (Kashiwagi et al 2012), and histone acetyltransferase inhibitor procyanidin B3 (Choi et al 2011).…”

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confidence: 99%

PMA induces androgen receptor downregulation and cellular apoptosis in prostate cancer cells

Itsumi

Shiota

Yokomizo

et al. 2014

Journal of Molecular Endocrinology

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Phorbol 12-myristate 13-acetate (PMA) induces cellular apoptosis in prostate cancer cells, the growth of which is governed by androgen/androgen receptor (AR) signaling, but the mechanism by which PMA exerts this effect remains unknown. Therefore, in this study, we investigated the mechanistic action of PMA in prostate cancer cells with regard to AR. We showed that PMA decreased E2F1 as well as AR expression in androgen-dependent prostate cancer LNCaP cells. Furthermore, PMA activated JNK and p53 signaling, resulting in the induction of cellular apoptosis. In LNCaP cells, androgen deprivation and a novel anti-androgen enzalutamide (MDV3100) augmented cellular apoptosis induced by PMA. Moreover, castration-resistant prostate cancer (CRPC) C4-2 cells were more sensitive to PMA compared with LNCaP cells and were sensitized to PMA by enzalutamide. Finally, the expression of PKC, E2F1, and AR was diminished in PMA-resistant cells, indicating that the gain of independence from PKC, E2F1, and AR functions leads to PMA resistance. In conclusion, PMA exerted its anti-cancer effects via the activation of pro-apoptotic JNK/p53 and inhibition of pro-proliferative E2F1/AR in prostate cancer cells including CRPC cells. The therapeutic effects of PMA were augmented by androgen deletion and enzalutamide in androgen-dependent prostate cancer cells, as well as by enzalutamide in castrationresistant cells. Taken together, PMA derivatives may be promising therapeutic agents for treating prostate cancer patients including CRPC patients.

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confidence: 99%

PMA induces androgen receptor downregulation and cellular apoptosis in prostate cancer cells

Itsumi

Shiota

Yokomizo

et al. 2014

Journal of Molecular Endocrinology

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“…Pro-B3 was reported to suppress cell proliferation through inhibition of p300-mediated AR acetylation both in vitro and in vivo in prostate cancer cells [190]. …”

Section: Regulation Of Nutrients On Histone Modification In Cancermentioning

confidence: 99%

Impact of Epigenetic Dietary Components on Cancer through Histone Modifications

Gao¹,

Tollefsbol

2015

CMC

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Epigenetics, the study of heritable changes in gene expression without modifying the nucleotide sequence, is among the most important topics in medicinal chemistry and cancer chemoprotection. Among those changes, DNA methylation and histone modification have been shown to be associated with various types of cancers in a number of ways, many of which are regulated by dietary components that are mostly found in plants. Although, mechanisms of nutrient components affecting histone acetylation/deacetylation in cancer are widely studied, how those natural compounds affect cancer through other histone modifications, such as methylation, phosphorylation and ubiquitylation, is rarely reviewed. Thus, this review article discusses impacts recently studied on histone acetylation as well as other histone modifications by dietary components, such as genistein, resveratrol, curcumin, epigallocatechin-3-gallate (EGCG), 3,3′-diindolylmethane (DIM), diallyl disulfide, garcinol, procyanidin B3, quercetin, sulforaphane and other isothiocyanates, in various types of cancer.

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“…For example, reduction of symptoms have been documented with the use of curcumin [16], extract of green tea [17], and extra virgin olive oil [18]. As a part of this group of generally recognized as safe (GRAS) plant-based products, procyanidins are a family of plant metabolites found in fruits, vegetables, nuts, seeds, flowers, and bark that have been shown to have beneficial biological activities, including anti-oxidative [19,20,21], anti-cancer [22,23,24], and vasorelaxing effects [25,26,27]. The composition of procyanidins include catechin, epicatechin, procyanidins B1–B5 and procyanidin C1 [28].…”

Section: Introductionmentioning

confidence: 99%

Procyanidins Mitigate Osteoarthritis Pathogenesis by, at Least in Part, Suppressing Vascular Endothelial Growth Factor Signaling

Wang

Leong

et al. 2016

IJMS

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Procyanidins are a family of plant metabolites that have been suggested to mitigate osteoarthritis pathogenesis in mice. However, the underlying mechanism is largely unknown. This study aimed to determine whether procyanidins mitigate traumatic injury-induced osteoarthritis (OA) disease progression, and whether procyanidins exert a chondroprotective effect by, at least in part, suppressing vascular endothelial growth factor signaling. Procyanidins (extracts from pine bark), orally administered to mice subjected to surgery for destabilization of the medial meniscus, significantly slowed OA disease progression. Real-time polymerase chain reaction revealed that procyanidin treatment reduced expression of vascular endothelial growth factor and effectors in OA pathogenesis that are regulated by vascular endothelial growth factor. Procyanidin-suppressed vascular endothelial growth factor expression was correlated with reduced phosphorylation of vascular endothelial growth factor receptor 2 in human OA primary chondrocytes. Moreover, components of procyanidins, procyanidin B2 and procyanidin B3 exerted effects similar to those of total procyanidins in mitigating the OA-related gene expression profile in the primary culture of human OA chondrocytes in the presence of vascular endothelial growth factor. Together, these findings suggest procyanidins mitigate OA pathogenesis, which is mediated, at least in part, by suppressing vascular endothelial growth factor signaling.

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Procyanidin B3, an inhibitor of histone acetyltransferase, enhances the action of antagonist for prostate cancer cells via inhibition of p300-dependent acetylation of androgen receptor

Cited by 54 publications

References 30 publications

PMA induces androgen receptor downregulation and cellular apoptosis in prostate cancer cells

PMA induces androgen receptor downregulation and cellular apoptosis in prostate cancer cells

Impact of Epigenetic Dietary Components on Cancer through Histone Modifications

Procyanidins Mitigate Osteoarthritis Pathogenesis by, at Least in Part, Suppressing Vascular Endothelial Growth Factor Signaling

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