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Article ; Online: Beyond Expression: Role of Phosphorylated Residues of EZH2 in Lineage Plasticity in Prostate Cancer.

Nouruzi, Shaghayegh / Tabrizian, Nakisa / Zoubeidi, Amina

2023 Volume 164, Issue 4

Abstract: Despite the development of effective targeted therapies and a significant understanding of carcinogenesis and cancer progression, treatment resistance is a major obstacle in achieving durable long-term control in many types of cancers. Emerging evidence ... ...

Abstract	Despite the development of effective targeted therapies and a significant understanding of carcinogenesis and cancer progression, treatment resistance is a major obstacle in achieving durable long-term control in many types of cancers. Emerging evidence supports that nongenetic mechanisms could play an underappreciated role in therapy resistance. These mechanisms include phenotypic plasticity, which is recognized as a hallmark of cancer and translates to epigenetic and transcriptional control of gene expression. Alterations in the expression and activity of the epigenetic modifier enhancer of zeste homolog 2 (EZH2) support prostate cancer lineage plasticity and progression. EZH2 expression and activity is elevated in castration-resistant prostate cancer treated with androgen receptor pathway inhibitors and in treatment-resistant prostate cancer. Moreover, 17 known residues of EZH2 are phosphorylated on by multiple kinases that modulate its activity, localization, stability, and polycomb repressive complex (PRC2) assembly. In this review, we explore the contribution of EZH2 phosphorylation in regulating canonical PRC2 in a methylation-dependent manner as an epigenetic repressor and in a noncanonical manner independent of PRC2 as a transcription activator. Apart from the contribution of EZH2 phosphorylation at serine 21, threonine 350, and threonine 311 in prostate cancer progression and treatment resistance, we discuss how other EZH2 phosphorylated residues with unknown functions could contribute to prostate cancer based on their upstream regulators and potential therapeutic utility.
MeSH term(s)	Male ; Humans ; Enhancer of Zeste Homolog 2 Protein/genetics ; Polycomb Repressive Complex 2/genetics ; Prostatic Neoplasms/metabolism ; Methylation ; Carcinogenesis/genetics ; Gene Expression Regulation, Neoplastic
Chemical Substances	Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; Polycomb Repressive Complex 2 (EC 2.1.1.43) ; EZH2 protein, human (EC 2.1.1.43)
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqad023
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Article ; Online: Targeting androgen receptor signaling: a historical perspective.

Davies, Alastair H / Zoubeidi, Amina

Endocrine-related cancer

2021 Volume 28, Issue 8, Page(s) T11–T18

Abstract: The first case of prostate cancer was identified by histological examination by Adams, a surgeon at The London Hospital, in 1853. In his report, Adams noted that the condition was 'a very rare disease'. Now, over 150 years later, with increased life ... ...

Abstract	The first case of prostate cancer was identified by histological examination by Adams, a surgeon at The London Hospital, in 1853. In his report, Adams noted that the condition was 'a very rare disease'. Now, over 150 years later, with increased life expectancy and screening, prostate cancer has become one of the most common cancers in men. In the United States alone, nearly 200,000 men are diagnosed with prostate cancer annually and about 33,000 succumb to their disease. Fifty years ago, men were typically diagnosed with prostate cancer in their seventies with disease that had metastasized to the bone and/or soft tissue. Diagnosis at such an advanced stage was a death sentence, with patients dying within 2 years. The pioneering work of Charles Huggins in the 1940s found that metastatic prostate cancer responds to androgen deprivation therapy (ADT), ushering in the rational use of hormone therapies that have irrevocably changed the course of prostate cancer disease management. Medical castration was the first effective systemic targeted therapy for any cancer and, to this day, androgen ablation remains the mainstay of prostate cancer therapy.
MeSH term(s)	Androgen Antagonists ; Androgens ; Humans ; Male ; Prostatic Neoplasms/pathology ; Receptors, Androgen
Chemical Substances	Androgen Antagonists ; Androgens ; Receptors, Androgen
Language	English
Publishing date	2021-07-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1530/ERC-21-0116
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Zs.A 4192: Show issues

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Article ; Online: Celebrating the 80th anniversary of hormone ablation for prostate cancer.

Zoubeidi, Amina / Ghosh, Paramita M

Endocrine-related cancer

2021 Volume 28, Issue 8, Page(s) T1–T10

Abstract: In this issue of Endocrine-Related Cancer, we are celebrating the 80th anniversary of hormone ablation as treatment for metastatic prostate cancer. Our understanding has evolved from the observation that androgen withdrawal, either surgical or ... ...

Abstract	In this issue of Endocrine-Related Cancer, we are celebrating the 80th anniversary of hormone ablation as treatment for metastatic prostate cancer. Our understanding has evolved from the observation that androgen withdrawal, either surgical or pharmacological, resulted in prostatic atrophy in animal models, to its application in patients, to investigation of the mysterious way in which prostate cancer escapes androgen dependence. We are now in an era of novel AR pathway inhibitors, the combination of androgen ablation with chemotherapy, PARP inhibitors, immunotherapies, guided radiotherapy, and novel drug application based upon genetic testing of individual tumors. In this special issue, we bring together a collection of eight reviews that cover not only the history of 80 years of progress after the initial identification of androgen ablation as an effective treatment of prostate cancer, but subsequent improvements in the understanding of the biology of the disease, development of novel treatment paradigms, resistance to those treatments and disease progression following that resistance.
MeSH term(s)	Androgen Antagonists/therapeutic use ; Androgen Receptor Antagonists/therapeutic use ; Androgens/metabolism ; Animals ; Anniversaries and Special Events ; Humans ; Male ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Receptors, Androgen/metabolism
Chemical Substances	Androgen Antagonists ; Androgen Receptor Antagonists ; Androgens ; Receptors, Androgen
Language	English
Publishing date	2021-07-15
Publishing country	England
Document type	Introductory Journal Article
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1530/ERC-21-0192
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Zs.A 4192: Show issues

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Article ; Online: The Transcriptional and Epigenetic Landscape of Cancer Cell Lineage Plasticity.

Davies, Alastair / Zoubeidi, Amina / Beltran, Himisha / Selth, Luke A

Cancer discovery

2023 Volume 13, Issue 8, Page(s) 1771–1788

Abstract: Lineage plasticity, a process whereby cells change their phenotype to take on a different molecular and/or histologic identity, is a key driver of cancer progression and therapy resistance. Although underlying genetic changes within the tumor can enhance ...

Abstract	Lineage plasticity, a process whereby cells change their phenotype to take on a different molecular and/or histologic identity, is a key driver of cancer progression and therapy resistance. Although underlying genetic changes within the tumor can enhance lineage plasticity, it is predominantly a dynamic process controlled by transcriptional and epigenetic dysregulation. This review explores the transcriptional and epigenetic regulators of lineage plasticity and their interplay with other features of malignancy, such as dysregulated metabolism, the tumor microenvironment, and immune evasion. We also discuss strategies for the detection and treatment of highly plastic tumors. Significance: Lineage plasticity is a hallmark of cancer and a critical facilitator of other oncogenic features such as metastasis, therapy resistance, dysregulated metabolism, and immune evasion. It is essential that the molecular mechanisms of lineage plasticity are elucidated to enable the development of strategies to effectively target this phenomenon. In this review, we describe key transcriptional and epigenetic regulators of cancer cell plasticity, in the process highlighting therapeutic approaches that may be harnessed for patient benefit.
MeSH term(s)	Humans ; Cell Lineage/genetics ; Cell Plasticity/genetics ; Neoplasms/genetics ; Epigenesis, Genetic ; Tumor Microenvironment/genetics
Language	English
Publishing date	2023-07-13
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-23-0225
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Zs.A 6916: Show issues

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Article ; Online: Co-targeting driver pathways in prostate cancer: two birds with one stone.

Zoubeidi, Amina / Gleave, Martin E

EMBO molecular medicine

2018 Volume 10, Issue 4

MeSH term(s)	Humans ; Male ; Prostatic Neoplasms ; Proto-Oncogene Proteins c-akt ; Signal Transduction ; TOR Serine-Threonine Kinases
Chemical Substances	MTOR protein, human (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2018-03-15
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.201808928
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Zs.A 6784: Show issues

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Article: Neural Transcription Factors in Disease Progression.

Thaper, Daksh / Vahid, Sepideh / Zoubeidi, Amina

Advances in experimental medicine and biology

2020 Volume 1210, Page(s) 437–462

Abstract: Progression to the malignant state is fundamentally dependent on transcriptional regulation in cancer cells. Optimum abundance of cell cycle proteins, angiogenesis factors, immune evasion markers, etc. is needed for proliferation, metastasis or ... ...

Abstract	Progression to the malignant state is fundamentally dependent on transcriptional regulation in cancer cells. Optimum abundance of cell cycle proteins, angiogenesis factors, immune evasion markers, etc. is needed for proliferation, metastasis or resistance to treatment. Therefore, dysregulation of transcription factors can compromise the normal prostate transcriptional network and contribute to malignant disease progression.The androgen receptor (AR) is considered to be a key transcription factor in prostate cancer (PCa) development and progression. Consequently, androgen pathway inhibitors (APIs) are currently the mainstay in PCa treatment, especially in castration-resistant prostate cancer (CRPC). However, emerging evidence suggests that with increased administration of potent APIs, prostate cancer can progress to a highly aggressive disease that morphologically resembles small cell carcinoma, which is referred to as neuroendocrine prostate cancer (NEPC), treatment-induced or treatment-emergent small cell prostate cancer. This chapter will review how neuronal transcription factors play a part in inducing a plastic stage in prostate cancer cells that eventually progresses to a more aggressive state such as NEPC.
MeSH term(s)	Carcinoma, Neuroendocrine/drug therapy ; Carcinoma, Neuroendocrine/genetics ; Carcinoma, Neuroendocrine/pathology ; Cell Cycle Proteins/metabolism ; Disease Progression ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Male ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Receptors, Androgen/metabolism ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/metabolism
Chemical Substances	Cell Cycle Proteins ; Receptors, Androgen ; Transcription Factors
Language	English
Publishing date	2020-01-03
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-32656-2_19
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Article ; Online: Reciprocal deregulation of NKX3.1 and AURKA axis in castration-resistant prostate cancer and NEPC models.

Sooreshjani, Moloud Aflaki / Kamra, Mohini / Zoubeidi, Amina / Shah, Kavita

Journal of biomedical science

2021 Volume 28, Issue 1, Page(s) 68

Abstract: Background: NKX3.1, a prostate-specific tumor suppressor, is either genomically lost or its protein levels are severely downregulated, which are invariably associated with poor prognosis in prostate cancer (PCa). Nevertheless, a clear disconnect exists ... ...

Abstract	Background: NKX3.1, a prostate-specific tumor suppressor, is either genomically lost or its protein levels are severely downregulated, which are invariably associated with poor prognosis in prostate cancer (PCa). Nevertheless, a clear disconnect exists between its mRNA and protein levels, indicating that its post-translational regulation may be critical in maintaining its protein levels. Similarly, AURKA is vastly overexpressed in all stages of prostate cancer (PCa), including castration-resistant PCa (CRPC) and neuroendocrine PCa (NEPC), although its transcripts are only increased in ~ 15% of cases, hinting at additional mechanisms of deregulation. Thus, identifying the upstream regulators that control AURKA and NKX3.1's levels and/or their downstream effectors offer an alternative route to inhibit AURKA and upregulate NKX3.1 in highly fatal CRPC and NEPC. AURKA and NKX3.1 have not linked to each other in any study to date. Methods: A chemical genetic screen revealed NKX3.1 as a direct target of AURKA. AURKA-NKX3.1 cross-talk was analyzed using several biochemical techniques in CRPC and NEPC cells. Results: We uncovered a reciprocal loop between AURKA and NKX3.1 in CRPC and NEPC cells. We observed that AURKA-mediated NKX3.1 downregulation is a major mechanism that drives CRPC pathogenesis and NEPC differentiation. AURKA phosphorylates NKX3.1 at three sites, which degrades it, but AURKA does not regulate NKX3.1 mRNA levels. NKX3.1 degradation drives highly aggressive oncogenic phenotypes in cells. NKX3.1 also degrades AURKA in a feedback loop. NKX3.1-AURKA loop thus upregulates AKT, ARv7 and Androgen Receptor (AR)-signaling in tandem promoting highly malignant phenotypes. Just as importantly, we observed that NKX3.1 overexpression fully abolished synaptophysin and enolase expression in NEPC cells, uncovering a strong negative relationship between NKX3.1 and neuroendocrine phenotypes, which was further confirmed be measuring neurite outgrowth. While WT-NKX3.1 inhibited neuronal differentiation, 3A-NKX3.1 expression obliterated it. Conclusions: NKX3.1 loss could be a major mechanism causing AURKA upregulation in CRPC and NEPC and vice versa. NKX3.1 genomic loss requires gene therapy, nonetheless, targeting AURKA provides a powerful tool to maintain NKX3.1 levels. Conversely, when NKX3.1 upregulation strategy using small molecules comes to fruition, AURKA inhibition should work synergistically due to the reciprocal loop in these highly aggressive incurable diseases.
MeSH term(s)	Aurora Kinase A/genetics ; Aurora Kinase A/metabolism ; Castration ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Male ; Prostatic Neoplasms/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Homeodomain Proteins ; NKX3-1 protein, human ; Transcription Factors ; AURKA protein, human (EC 2.7.11.1) ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2021-10-08
Publishing country	England
Document type	Journal Article
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-021-00765-z
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Zs.A 4037: Show issues

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Article ; Online: Clusterin as a therapeutic target.

Wilson, Mark R / Zoubeidi, Amina

Expert opinion on therapeutic targets

2017 Volume 21, Issue 2, Page(s) 201–213

Abstract: Introduction: Clusterin (CLU) is a stress-activated, ATP-independent molecular chaperone, normally secreted from cells, that is up-regulated in Alzheimer disease and in many cancers. It plays important roles in protein homeostasis/proteostasis, ... ...

Abstract	Introduction: Clusterin (CLU) is a stress-activated, ATP-independent molecular chaperone, normally secreted from cells, that is up-regulated in Alzheimer disease and in many cancers. It plays important roles in protein homeostasis/proteostasis, inhibition of cell death pathways, and modulation of pro-survival signalling and transcriptional networks. Changes in the CLU gene locus are highly associated with Alzheimer disease, and many therapy-resistant cancers over-express CLU. The extensive post-translational processing and heterogeneous oligomerization of CLU have so far prevented any definitive structure determination. This in turn has meant that targeting CLU with small molecule inhibitors is challenging. Therefore, inhibiting CLU at the gene-expression level using siRNA or antisense is a valid approach to inhibit its function. Areas covered: This article reviews recent advances regarding the role of CLU in proteostasis, cellular trafficking, human diseases, and signalling pathways involved in oncogenesis. It addresses the rationale for CLU as a therapeutic target in cancer, and the current status of pre-clinical and clinical studies using CLU antisense inhibitor OGX011. Expert opinion: Discusses challenges facing the therapeutic targeting of CLU including rapid changes in the treatment landscape for prostate cancer with multiple new FDA approved drugs, selection of windows of intervention, and potential side effects when silencing CLU expression.
MeSH term(s)	Animals ; Clusterin/genetics ; Drug Design ; Gene Expression Regulation/genetics ; Humans ; Male ; Molecular Targeted Therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy ; RNA, Small Interfering/administration & dosage ; Signal Transduction ; Thionucleotides/pharmacology
Chemical Substances	Clusterin ; OGX-011 ; RNA, Small Interfering ; Thionucleotides
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1080/14728222.2017.1267142
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Zs.A 5244: Show issues

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Article ; Online: Biological Evolution of Castration-resistant Prostate Cancer.

Davies, Alastair / Conteduca, Vincenza / Zoubeidi, Amina / Beltran, Himisha

European urology focus

2019 Volume 5, Issue 2, Page(s) 147–154

Abstract: Context: Recent studies focused on the molecular characterization of metastatic prostate cancer have identified genomic subsets and emerging resistance patterns. Detection of these alterations in patients has potential implications for therapy selection ...

Abstract	Context: Recent studies focused on the molecular characterization of metastatic prostate cancer have identified genomic subsets and emerging resistance patterns. Detection of these alterations in patients has potential implications for therapy selection and prognostication. Objective: The primary objective is to review the current landscape of clinical and molecular biomarkers in advanced prostate cancer and understand how they may reflect underlying tumor biology. We also discuss how these features may potentially impact earlier stages of the disease. Evidence acquisition: A literature search was performed of recent clinical biomarker/genomic studies focused on advanced metastatic prostate cancer as well as relevant preclinical studies investigating how these alterations influence therapy response or resistance. Evidence synthesis: Metastatic castration-resistant prostate cancer is commonly driven by androgen receptor signaling even after progression on potent hormonal agents, but other alterations may also be present or emerge during therapy resistance such as DNA repair gene aberrations or combined loss of tumor suppressor genes. Biological implications of these changes are context dependent, which may affect their detection and interpretation. Conclusions: Molecular changes occur during prostate cancer progression and treatment resistance. Detection of genomic alterations has potential to influence therapy choice. Additional studies are warranted to elucidate the evolution of these changes and their impact in earlier stages of the disease. Patient summary: We review the biology of advanced prostate cancer, and highlight opportunities and challenges for using biological or molecular assays to help guide individualized treatment decisions for patients.
MeSH term(s)	Androgen Antagonists/therapeutic use ; Biomarkers/metabolism ; Disease Progression ; Genomics/methods ; Humans ; Male ; Molecular Biology/methods ; Neoplasm Metastasis/pathology ; Prognosis ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Prostatic Neoplasms, Castration-Resistant/secondary ; Receptors, Androgen/drug effects ; Receptors, Androgen/genetics
Chemical Substances	Androgen Antagonists ; Biomarkers ; Receptors, Androgen
Language	English
Publishing date	2019-02-14
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ISSN	2405-4569
ISSN (online)	2405-4569
DOI	10.1016/j.euf.2019.01.016
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Article ; Online: The epigenetic and transcriptional landscape of neuroendocrine prostate cancer.

Davies, Alastair / Zoubeidi, Amina / Selth, Luke A

Endocrine-related cancer

2019 Volume 27, Issue 2, Page(s) R35–R50

Abstract: Tumours adapt to increasingly potent targeted therapies by transitioning to alternative lineage states. In prostate cancer, the widespread clinical application of androgen receptor (AR) pathway inhibitors has led to the insurgence of tumours relapsing ... ...

Abstract	Tumours adapt to increasingly potent targeted therapies by transitioning to alternative lineage states. In prostate cancer, the widespread clinical application of androgen receptor (AR) pathway inhibitors has led to the insurgence of tumours relapsing with a neuroendocrine phenotype, termed neuroendocrine prostate cancer (NEPC). Recent evidence suggests that this lineage reprogramming is driven largely by dysregulation of the epigenome and transcriptional networks. Indeed, aberrant DNA methylation patterning and altered expression of epigenetic modifiers, such as EZH2, transcription factors, and RNA-modifying factors, are hallmarks of NEPC tumours. In this review, we explore the nature of the epigenetic and transcriptional landscape as prostate cancer cells lose their AR-imposed identity and transition to the neuroendocrine lineage. Beyond addressing the mechanisms underlying epithelial-to-neuroendocrine lineage reprogramming, we discuss how oncogenic signaling and metabolic shifts fuel epigenetic/transcriptional changes as well as the current state of epigenetic therapies for NEPC.
MeSH term(s)	Epigenesis, Genetic ; Gene Regulatory Networks ; Humans ; Male ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Transcriptome
Language	English
Publishing date	2019-12-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1530/ERC-19-0420
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