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Article ; Online: Targeting constitutive NF-κB specifically in tumor cells.

Jeong, Ji-Hak / Dickinson, Shohreh Iravani / Luo, Jun-Li

2017 Volume 8, Issue 55, Page(s) 93305–93306

Language	English
Publishing date	2017-11-07
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.22069
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Article ; Online: Premalignant and malignant prostate lesions: pathologic review.

Dickinson, Shohreh Iravani

Cancer control : journal of the Moffitt Cancer Center

2010 Volume 17, Issue 4, Page(s) 214–222

Abstract: Background: High-grade prostatic intraepithelial neoplasia (HGPIN) is currently the only recognized premalignant lesion of prostatic carcinoma.: Methods: This review article discusses HGPIN, its link to prostatic adenocarcinoma, and the significance ... ...

Abstract	Background: High-grade prostatic intraepithelial neoplasia (HGPIN) is currently the only recognized premalignant lesion of prostatic carcinoma. Methods: This review article discusses HGPIN, its link to prostatic adenocarcinoma, and the significance of its presence on needle biopsy. The criteria and clinical impact of the diagnosis of atypical small acinar proliferation on needle biopsy are reviewed. Certain subtypes of prostate cancer that are not associated with HGPIN are of clinical relevance, and the unique clinicopathologic features of these subtypes are discussed. Histologic variants of prostatic adenocarcinoma with distinct cell types are also described. Results: HGPIN is the only known pathologic factor currently available to distinguish which patients may be at risk for detecting carcinoma on repeat biopsy. Histologic variants are recognized due to the inference of a particular Gleason grade pattern associated with the cell type, hence affecting prognosis. Typically, pure forms of these histologic variants are associated with worse prognosis due to the associated high Gleason grades. Conclusions: HGPIN has a strong association with acinar-type prostatic adenocarcinoma. HGPIN and acinar-type prostatic adenocarcinoma both show similar molecular alterations, providing further evidence of their association.
MeSH term(s)	Adenocarcinoma/pathology ; Biopsy, Needle ; Carcinoma, Acinar Cell/pathology ; Humans ; Male ; Neoplasm Staging ; Prognosis ; Prostatic Intraepithelial Neoplasia/pathology ; Prostatic Neoplasms/pathology
Language	English
Publishing date	2010-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1328503-8
ISSN	1526-2359 ; 1073-2748
ISSN (online)	1526-2359
ISSN	1073-2748
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Article ; Online: Targeting INMT and interrupting its methylation pathway for the treatment of castration resistant prostate cancer.

Zhong, Shangwei / Jeong, Ji-Hak / Huang, Changhao / Chen, Xueyan / Dickinson, Shohreh Iravani / Dhillon, Jasreman / Yang, Li / Luo, Jun-Li

Journal of experimental & clinical cancer research : CR

2021 Volume 40, Issue 1, Page(s) 307

Abstract: Background: Castration-resistant prostate cancer (CRPC) is associated with a very poor prognosis, and the treatment of which remains a serious clinical challenge.: Methods: RNA-seq, qPCR, western blot and immunohistochemistry were employed to ... ...

Abstract	Background: Castration-resistant prostate cancer (CRPC) is associated with a very poor prognosis, and the treatment of which remains a serious clinical challenge. Methods: RNA-seq, qPCR, western blot and immunohistochemistry were employed to identify and confirm the high expression of indolethylamine N-methyltransferase (INMT) in CRPC and the clinical relevance. Chip assay was used to identify Histone-Lysine N-Methyltransferase (SMYD3) as a major epigenetic regulator of INMT. LC-MS/MS were used to identify new substrates of INMT methylation in CRPC tissues. Gene knockdown/overexpression, MTT and mouse cancer models were used to examine the role of INMT as well as the anticancer efficacy of INMT inhibitor N,N-dimethyltryptamine (DMT), the SMYD3 inhibitor BCl-12, the selenium compounds methaneseleninic acid (MSA) and Se-(Methyl)selenocysteine hydrochloride (MSC), and the newly identified endogenous INMT substrate Bis(7)-tacrine. Results: We found that the expression of INMT was highly increased in CRPC and was correlated with poor prognosis of clinical prostate cancer (PCa). INMT promoted PCa castration resistance via detoxification of anticancer metabolites. Knockdown of INMT or treatment with INMT inhibitor N,N-dimethyltryptamine (DMT) significantly suppressed CRPC development. Histone-Lysine N-Methyltransferase SMYD3 was a major epigenetic regulator of INMT expression, treatment with SMYD3 inhibitor BCl-121 suppressed INMT expression and inhibits CRPC development. Importantly, INMT knockdown significantly increased the anticancer effect of the exogenous selenium compounds methaneseleninic acid (MSA) and Se-(Methyl)selenocysteine hydrochloride (MSC) as well as the endogenous metabolite Bis(7)-tacrine. Conclusions: Our study suggests that INMT drives PCa castration resistance through detoxification of anticancer metabolites, targeting INMT or its regulator SMYD3 or/and its methylation metabolites represents an effective therapeutic avenue for CRPC treatment.
MeSH term(s)	Animals ; Apoptosis ; Cell Proliferation ; DNA Methylation ; Enzyme Inhibitors/pharmacology ; Epigenesis, Genetic ; Gene Expression Regulation, Enzymologic/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Histone-Lysine N-Methyltransferase/antagonists & inhibitors ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Humans ; Male ; Methyltransferases/antagonists & inhibitors ; Mice ; Prognosis ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/enzymology ; Prostatic Neoplasms, Castration-Resistant/pathology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Enzyme Inhibitors ; Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; SMYD3 protein, human (EC 2.1.1.43) ; tryptamine N-methyltransferase (EC 2.1.1.49)
Language	English
Publishing date	2021-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-021-02109-z
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Article ; Online: A Constitutive Intrinsic Inflammatory Signaling Circuit Composed of miR-196b, Meis2, PPP3CC, and p65 Drives Prostate Cancer Castration Resistance.

Jeong, Ji-Hak / Park, Sun-Jin / Dickinson, Shohreh Iravani / Luo, Jun-Li

Molecular cell

2017 Volume 65, Issue 1, Page(s) 154–167

Abstract: Androgen deprivation therapy is the most effective treatment for advanced prostate cancer, but almost all cancer eventually becomes castration resistant, and the underlying mechanisms are largely unknown. Here, we show that an intrinsic constitutively ... ...

Abstract	Androgen deprivation therapy is the most effective treatment for advanced prostate cancer, but almost all cancer eventually becomes castration resistant, and the underlying mechanisms are largely unknown. Here, we show that an intrinsic constitutively activated feedforward signaling circuit composed of IκBα/NF-κB(p65), miR-196b-3p, Meis2, and PPP3CC is formed during the emergence of castration-resistant prostate cancer (CRPC). This circuit controls the expression of stem cell transcription factors that drives the high tumorigenicity of CRPC cells. Interrupting the circuit by targeting its individual components significantly impairs the tumorigenicity and CRPC development. Notably, constitutive activation of IκBα/NF-κB(p65) in this circuit is not dependent on the activation of traditional IKKβ/NF-κB pathways that are important in normal immune responses. Therefore, our studies present deep insight into the bona fide mechanisms underlying castration resistance and provide the foundation for the development of CRPC therapeutic strategies that would be highly efficient while avoiding indiscriminate IKK/NF-κB inhibition in normal cells.
MeSH term(s)	Androgen Antagonists/pharmacology ; Animals ; Antineoplastic Agents, Hormonal/pharmacology ; Calcineurin/genetics ; Calcineurin/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Drug Resistance, Neoplasm ; Gene Expression Regulation, Neoplastic ; Genes, myc ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Male ; Mice, Transgenic ; MicroRNAs/genetics ; MicroRNAs/metabolism ; NF-KappaB Inhibitor alpha/genetics ; NF-KappaB Inhibitor alpha/metabolism ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Phenotype ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Prostatic Neoplasms, Castration-Resistant/pathology ; RNA Interference ; Signal Transduction ; Time Factors ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transfection ; Tumor Burden ; Tumor Cells, Cultured
Chemical Substances	Androgen Antagonists ; Antineoplastic Agents, Hormonal ; Homeodomain Proteins ; MEIS2 protein, human ; MIRN196 microRNA, human ; MIRN196 microRNA, mouse ; MicroRNAs ; Mrg1 protein, mouse ; NFKBIA protein, human ; Nfkbia protein, mouse ; RELA protein, human ; Rela protein, mouse ; Transcription Factor RelA ; Transcription Factors ; RAG-1 protein (128559-51-3) ; NF-KappaB Inhibitor alpha (139874-52-5) ; Calcineurin (EC 3.1.3.16) ; PPP3CC protein, human (EC 3.1.3.16) ; PPP3CC protein, mouse (EC 3.1.3.16)
Language	English
Publishing date	2017-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2016.11.034
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Article: A Constitutive Intrinsic Inflammatory Signaling Circuit Composed of miR-196b, Meis2, PPP3CC, and p65 Drives Prostate Cancer Castration Resistance

Jeong, Ji-Hak / Jun-Li Luo / Shohreh Iravani Dickinson / Sun-Jin Park

Molecular cell. 2017 Jan. 05, v. 65, no. 1

2017

Abstract	Androgen deprivation therapy is the most effective treatment for advanced prostate cancer, but almost all cancer eventually becomes castration resistant, and the underlying mechanisms are largely unknown. Here, we show that an intrinsic constitutively activated feedforward signaling circuit composed of IκBα/NF-κB(p65), miR-196b-3p, Meis2, and PPP3CC is formed during the emergence of castration-resistant prostate cancer (CRPC). This circuit controls the expression of stem cell transcription factors that drives the high tumorigenicity of CRPC cells. Interrupting the circuit by targeting its individual components significantly impairs the tumorigenicity and CRPC development. Notably, constitutive activation of IκBα/NF-κB(p65) in this circuit is not dependent on the activation of traditional IKKβ/NF-κB pathways that are important in normal immune responses. Therefore, our studies present deep insight into the bona fide mechanisms underlying castration resistance and provide the foundation for the development of CRPC therapeutic strategies that would be highly efficient while avoiding indiscriminate IKK/NF-κB inhibition in normal cells.
Keywords	castration ; immune response ; prostatic neoplasms ; stem cells ; transcription factors
Language	English
Dates of publication	2017-0105
Size	p. 154-167.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2016.11.034
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Expression and function of SIRT6 in muscle invasive urothelial carcinoma of the bladder.

Wu, Minghui / Dickinson, Shohreh Iravani / Wang, Xue / Zhang, Jingsong

International journal of clinical and experimental pathology

2014 Volume 7, Issue 10, Page(s) 6504–6513

Abstract: SIRT6, a member of the class III histone deacetylase, has been shown to inhibit glycolysis and promote DNA double strand break repairs. Despite of its proposed tumor suppressor role, no significant differences in SIRT6 mRNA levels among normal bladder ... ...

Abstract	SIRT6, a member of the class III histone deacetylase, has been shown to inhibit glycolysis and promote DNA double strand break repairs. Despite of its proposed tumor suppressor role, no significant differences in SIRT6 mRNA levels among normal bladder urothelium, non-muscle invasive, and muscle invasive urothelial carcinoma were noted in the two largest bladder cancer gene expression datasets available in Oncomine. We therefore studied the expression and function of SIRT6 in muscle invasive urothelial carcinoma of the bladder. Immunohistochemistry studies of SIRT6 on radical cystectomy samples showed a dramatic decline of SIRT6 expression when bladder cancer progressed from T2 to T4. Functional study with bladder cancer cell lines confirmed its role in inhibiting glycolysis and cell proliferation. Reducing SIRT6 with siRNA, however, did not sensitize bladder cancer cells to drug induced DNA damage. The differential expression patterns of SIRT6 amongst different T stages of muscle invasive bladder cancers indicate less reliance on glycolysis when urothelial carcinoma invades deeper through the bladder and into the adjacent tissues.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Carcinoma/enzymology ; Carcinoma/genetics ; Carcinoma/pathology ; Carcinoma/surgery ; Cell Line, Tumor ; Cell Proliferation ; Cystectomy ; Glycolysis ; Humans ; Immunohistochemistry ; Muscle, Smooth/pathology ; Muscle, Smooth/surgery ; Neoplasm Invasiveness ; Neoplasm Staging ; RNA Interference ; Sirtuins/genetics ; Sirtuins/metabolism ; Time Factors ; Transfection ; Urinary Bladder Neoplasms/enzymology ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/pathology ; Urinary Bladder Neoplasms/surgery ; Urothelium/drug effects ; Urothelium/enzymology ; Urothelium/pathology ; Urothelium/surgery
Chemical Substances	Antineoplastic Agents ; SIRT6 protein, human (EC 3.5.1.-) ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2418306-4
ISSN	1936-2625 ; 1936-2625
ISSN (online)	1936-2625
ISSN	1936-2625
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Article ; Online: Bladder cancer: a review of non-muscle invasive disease.

Sexton, Wade J / Wiegand, Lucas R / Correa, José J / Politis, Christos / Dickinson, Shohreh Iravani / Kang, Loveleen C

Cancer control : journal of the Moffitt Cancer Center

2010 Volume 17, Issue 4, Page(s) 256–268

Abstract: Background: Bladder cancer is one of the most common cancers affecting men and women and thus has a profound impact on health care. The majority of patients (75%) with newly diagnosed urothelial tumors have non-muscle invasive disease confined to the ... ...

Abstract	Background: Bladder cancer is one of the most common cancers affecting men and women and thus has a profound impact on health care. The majority of patients (75%) with newly diagnosed urothelial tumors have non-muscle invasive disease confined to the bladder mucosa or the lamina propria. Methods: The authors review the literature as well as recently published clinical guidelines regarding the bladder cancer risk and causative factors, diagnostic and pathologic evaluation, prognostic variables, and management strategies for patients with non-muscle invasive bladder cancer. Results: Recurrence and progression remain problematic for many patients and are dependent on multiple clinical and pathological features, the most important of which are tumor stage, grade, multifocality, size, recurrence patterns, and the association with carcinoma in situ. Accurate assessment of clinical stage and tumor grade is critical in determining management and surveillance strategies. Intravesical therapies positively influence tumor recurrence rates. Disease progression rates may be impacted in high-risk patients who receive both induction bacille Calmette-Guérin (BCG) and a maintenance BCG regimen. Cystectomy still plays a pivotal role in patients with high-risk tumors and in patients who fail more conservative attempts to eradicate non-muscle invasive disease. Conclusions: Non-muscle invasive bladder cancers represent a broad group of tumors with varying biologic potential. Successful treatment depends on the careful integration of diagnostic and surveillance tests, macroablation through transurethral resection, accurate assessment of clinical stage, and the timely and appropriate delivery of intravesical chemotherapeutic and immunomodulatory agents.
MeSH term(s)	Administration, Intravesical ; Antineoplastic Agents/therapeutic use ; Combined Modality Therapy ; Disease Progression ; Humans ; Neoplasm Invasiveness ; Neoplasm Recurrence, Local ; Neoplasm Staging ; Risk Factors ; Urinary Bladder Neoplasms/diagnosis ; Urinary Bladder Neoplasms/pathology ; Urinary Bladder Neoplasms/therapy
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2010-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1328503-8
ISSN	1526-2359 ; 1073-2748
ISSN (online)	1526-2359
ISSN	1073-2748
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Article: Prostate Cancer Chemoprevention Targeting High Risk Populations: Model for Trial Design and Outcome Measures.

Kumar, Nagi / Crocker, Theresa / Smith, Tiffany / Pow-Sang, Julio / Spiess, Philippe E / Connors, Shanjayla / Chornukur, Ganna / Dickinson, Shohreh Iravani / Bai, Wenlong / Williams, Christopher R / Salup, Raoul / Fu, Wui

Journal of cancer science & therapy

2012 Volume 2011, Issue S3

Abstract: Inspite of the large number of promising nutrient-derived agents demonstrating promise as potential chemopreventive agents, most have failed to prove effectiveness in clinical trials. Critical requirements for moving nutrient-derived agents to ... ...

Abstract	Inspite of the large number of promising nutrient-derived agents demonstrating promise as potential chemopreventive agents, most have failed to prove effectiveness in clinical trials. Critical requirements for moving nutrient-derived agents to recommendation for clinical use include adopting a systematic, molecular-mechanism based approach and utilizing the same ethical and rigorous methods such as are used to evaluate other pharmacological agents. Preliminary data on a mechanistic rationale for chemoprevention activity as observed from epidemiological, in vitro and preclinical studies, phase I data of safety in high-risk cohorts are required to inform design of phase II clinical trials. Additionally, a valid panel of biomarkers representing the hypothesized carcinogenesis pathway for measuring efficacy must be utilized to evaluate effectiveness in these trials. The goal of this paper is to provide a model, using a systematic approach for evaluating the safety, effectiveness and mechanism of action of a well characterized nutrient-derived agent-isoflavones - in a phase II clinical trial for prostate cancer (CaP) chemoprevention, targeting a population of African American (AA) and Caucasian men. Based on our previous observations, we hypothesize that the effects of isoflavones on prostate carcinogenesis are mainly mediated through the down regulation of androgen receptor (AR) and AR activity in AA men is higher due to its shorter length of Glutamine repeats in its N-terminus. We thus believe that isoflavones will exert a stronger protective effect for CaP in AA men and cause a higher activation of FOXO factors and their target genes. The aim of the study is to evaluate the comparative effectiveness of the study agent and placebo, in addition to a comparison of the effectiveness and safety in African American men compared to Caucasian men treated with this agent.
Language	English
Publishing date	2012-01-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2578254-X
ISSN	1948-5956
ISSN	1948-5956
DOI	10.4172/1948-5956.s3-007
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