CREBBP/EP300 Bromodomain Inhibition Affects the Proliferation of AR-Positive Breast Cancer Cell Lines

García-Carpizo, Verónica; Ruiz‐Llorente, Sergio; Sarmentero, Jacinto; González-Corpas, Ana; Barrero, María J.

doi:10.1158/1541-7786.mcr-18-0719

Cited by 29 publications

(15 citation statements)

References 52 publications

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“…Moreover, almost half of the known BRD-containing proteins are related to PCa, which also contribute the main chromatin-related processes and changes in PCa, beyond BRD4 36 . These BRD-containing proteins (such as ATAD2, BRD8, CREBBP, and KTM2A) perform a wide range of downstream functions by recognizing acetylated histones, also present to be TFs, AR co-activators or methyltransferases [37][38][39] . Therefore, BRD-containing proteins are important transcriptional regulators that initiate chromatin restructuring beyond the SE function.…”

Section: Se-related Protein Bet/brd4 In Prostate Cancermentioning

confidence: 99%

Super-enhancer in prostate cancer: transcriptional disorders and therapeutic targets

Chen

Shang

et al. 2020

npj Precis. Onc.

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Abnormal activity of oncogenic and tumor-suppressor signaling pathways contributes to cancer and cancer risk in humans. Transcriptional dysregulation of these pathways is commonly associated with tumorigenesis and the development of cancer. Genetic and epigenetic alterations may mediate dysregulated transcriptional activity. One of the most important epigenetic alternations is the non-coding regulatory element, which includes both enhancers and super-enhancers (SEs). SEs, characterized as large clusters of enhancers with aberrant high levels of transcription factor binding, have been considered as key drivers of gene expression in controlling and maintaining cancer cell identity. In cancer cells, oncogenes acquire SEs and the cancer phenotype relies on these abnormal transcription programs driven by SEs, which leads to cancer cells often becoming addicted to the SEs-related transcription programs, including prostate cancer. Here, we summarize recent findings of SEs and SEs-related gene regulation in prostate cancer and review the potential pharmacological inhibitors in basic research and clinical trials.

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Section: Se-related Protein Bet/brd4 In Prostate Cancermentioning

confidence: 99%

Super-enhancer in prostate cancer: transcriptional disorders and therapeutic targets

Chen

Shang

et al. 2020

npj Precis. Onc.

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“…Since the squelching of EP300 by AR from ER-binding sites in ER+ BCa appears to be the prevalent crosstalk mechanism between the SRs ( Hickey et al 2021 ), the EP300 might act as an important regulator of AR’s action in BCa. Indeed, the activity of AR in TNBC is sensitive to the inhibition of EP300 ( Garcia-Carpizo et al 2019 ) ( Fig. 2D ).…”

Section: Breast Cancermentioning

confidence: 97%

Genome-wide crosstalk between steroid receptors in breast and prostate cancers

Paakinaho

2021

Endocrine-Related Cancer

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Steroid receptors (SRs) constitute an important class of signal-dependent transcription factors (TFs). They regulate a variety of key biological processes and are crucial drug targets in many disease states. In particular, estrogen (ER) and androgen receptors (AR) drive the development and progression of breast and prostate cancer, respectively. Thus, they represent the main specific drug targets in these diseases. Recent evidence has suggested that the crosstalk between signal-dependent TFs is an important step in the reprogramming of chromatin sites; a signal-activated TF can expand or restrict the chromatin binding of another TF. This crosstalk can rewire gene programs and thus alter biological processes and influence the progression of disease. Lately, it has been postulated that there may be an important crosstalk between the AR and the ER with other SRs. Especially, progesterone (PR) and glucocorticoid receptor (GR) can reprogram chromatin binding of ER and gene programs in breast cancer cells. Furthermore, GR can take the place of AR in antiandrogen-resistant prostate cancer cells. Here, we review the current knowledge of the crosstalk between SRs in breast and prostate cancers. We emphasize how the activity of ER and AR on chromatin can be modulated by other SRs on a genome-wide scale. We also highlight the knowledge gaps in the interplay of SRs and their complex interactions with other signaling pathways and suggest how to experimentally fill in these gaps.

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“…Characterization of breast cancer cell lines based on the receptors they express: Estrogen Receptor (ER), Progesterone Receptor (PR), Androgen Receptor (AR), and Human Epidermal Growth Factor Receptor 2 (HER2); and classification of the tumor they origin, into breast cancer subtypes depending on the receptors they express: Luminal A (LA), Luminal B (LB), HER2 Enriched (H), Triple-Negative A or basal-like (TNA), and Triple-Negative B or normal-like (TNB); and on their histopathological features: benign tumor (B), adenocarcinoma (AC), ductal carcinoma (DC), invasive ductal carcinoma (IDC), invasive lobular carcinoma (ILC), inflammatory carcinoma (InfC), inflammatory ductal carcinoma (InfDC), medullary carcinomas (MC), or squamous carcinoma (SqC). Additional information on the culture medias more commonly used for each cell line: Ham's F12 liquid medium (HAM's F12), Dulbecco's Modified Eagle's Medium (DMEM), Roswell Park Memorial Institute (RPMI) medium and Minimal Essential Medium Eagle-alpha modified with nucleosides and DFC1 medium (α-MEM/DFC1) [11,15,16,18,[66][67][68][69][70][71][72][73]. The receptors are considered present in the cells (+), absent (−), information still controversial (+/−), or there is still non-available information (NA).…”

Section: D Modelsmentioning

confidence: 99%

Experimental Models as Refined Translational Tools for Breast Cancer Research

et al. 2020

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Breast cancer is one of the most common cancers worldwide, which makes it a very impactful malignancy in the society. Breast cancers can be classified through different systems based on the main tumor features and gene, protein, and cell receptors expression, which will determine the most advisable therapeutic course and expected outcomes. Multiple therapeutic options have already been proposed and implemented for breast cancer treatment. Nonetheless, their use and efficacy still greatly depend on the tumor classification, and treatments are commonly associated with invasiveness, pain, discomfort, severe side effects, and poor specificity. This has demanded an investment in the research of the mechanisms behind the disease progression, evolution, and associated risk factors, and on novel diagnostic and therapeutic techniques. However, advances in the understanding and assessment of breast cancer are dependent on the ability to mimic the properties and microenvironment of tumors in vivo, which can be achieved through experimentation on animal models. This review covers an overview of the main animal models used in breast cancer research, namely in vitro models, in vivo models, in silico models, and other models. For each model, the main characteristics, advantages, and challenges associated to their use are highlighted.

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CREBBP/EP300 Bromodomain Inhibition Affects the Proliferation of AR-Positive Breast Cancer Cell Lines

Cited by 29 publications

References 52 publications

Super-enhancer in prostate cancer: transcriptional disorders and therapeutic targets

Super-enhancer in prostate cancer: transcriptional disorders and therapeutic targets

Genome-wide crosstalk between steroid receptors in breast and prostate cancers

Experimental Models as Refined Translational Tools for Breast Cancer Research

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