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Article ; Online: Could TNF-antagonists be a novel treatment strategy for BPH patients?

Vickman, Renee E / Franco, Omar E / Hayward, Simon W

Cell stress

2022 Volume 6, Issue 6, Page(s) 65–67

Abstract: Tumor necrosis factor (TNF) is widely recognized as a pivotal player in both systemic and local inflammatory processes. Due to the critical role this molecule has in driving both chronic and acute inflammation, it was among the earliest therapeutic ... ...

Abstract	Tumor necrosis factor (TNF) is widely recognized as a pivotal player in both systemic and local inflammatory processes. Due to the critical role this molecule has in driving both chronic and acute inflammation, it was among the earliest therapeutic targets utilized for patients with autoimmune (AI) diseases. While inflammation in the prostate is commonly observed, the organ has not previously been considered a target of systemic inflammation associated with some AI diseases. In patients with benign prostatic hyperplasia (BPH), chronic inflammation is common, and immune cells represent a significant proportion of cells in the organ. Accumulation of inflammatory cells may be a response to an initial insult and/or a factor in driving BPH pathogenesis. Certainly, inflammation can limit the efficacy of existing medical therapies in these patients. We previously showed that a pattern of gene expression in BPH tissues from patients who had progressed to indication-specific surgery was consistent with the changes seen in AI diseases. Recently, we demonstrated that patients with AI disease have an approximately 50% increase in BPH prevalence compared to patients without AI disease. Treatment of AI disease patients, specifically with TNF-antagonists, reduces BPH incidence back to, or in some diseases, below, the baseline population BPH diagnosis rate. Treatment of AI disease patients with the broad spectrum anti-inflammatory methotrexate did not elicit this reduction in diagnoses. Systemic treatment with TNF antagonists reduces epithelial proliferation and macrophage accumulation in the prostate tissues from two mouse models of prostatic hyperplasia as well as human patients. These studies suggest that TNF is a potential therapeutic target in BPH patients.
Language	English
Publishing date	2022-06-07
Publishing country	Austria
Document type	Journal Article ; Comment
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2022.06.268
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Article ; Online: Static and dynamic magnetic properties of circular and square cobalt nanodots in hexagonal cells.

Mélica, Franco N / Saavedra, Eduardo / Escrig, Juan / Bajales, Noelia / Linarez Pérez, Omar E / Arciniegas Jaimes, Diana M

Physical chemistry chemical physics : PCCP

2024 Volume 26, Issue 6, Page(s) 5621–5632

Abstract: In this work we performed a detailed numerical analysis to investigate the static and dynamic magnetic properties of hexagonal cells of square and circular cobalt nanodots as a function of the distance between them and the external magnetic field to ... ...

Abstract	In this work we performed a detailed numerical analysis to investigate the static and dynamic magnetic properties of hexagonal cells of square and circular cobalt nanodots as a function of the distance between them and the external magnetic field to which they are subjected. By simulating hysteresis curves with the external magnetic field applied parallel and perpendicular to the plane of these nanostructures, we can conclude that the cobalt nanodots presented a significant perpendicular magnetic anisotropy. We also obtained that the coercivity increases with decreasing volume, which implies that the circular dots have a higher coercivity than the square dots. Furthermore, we studied the dynamic susceptibility of these systems and found that it is possible to control both the position and the number of resonance peaks by controlling the geometry and the distance between the magnetic nanodots. This work provides useful information on the behaviour of cobalt nanodot arrays, opening paths for the design and improvement of two-dimensional technological devices.
Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1476244-4
ISSN	1463-9084 ; 1463-9076
ISSN (online)	1463-9084
ISSN	1463-9076
DOI	10.1039/d3cp05432b
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Article ; Online: Could TNF-antagonists be a novel treatment strategy for BPH patients?

Renee E. Vickman / Omar E. Franco / Simon W. Hayward

Cell Stress, Vol 6, Iss 6, Pp 65-

2022 Volume 67

Abstract	Tumor necrosis factor (TNF) is widely recognized as a pivotal player in both systemic and local inflammatory processes. Due to the critical role this molecule has in driving both chronic and acute inflammation, it was among the earliest therapeutic targets utilized for pa-tients with autoimmune (AI) diseases. While inflamma-tion in the prostate is commonly observed, the organ has not previously been considered a target of systemic inflammation associated with some AI diseases. In pa-tients with benign prostatic hyperplasia (BPH), chronic inflammation is common, and immune cells represent a significant proportion of cells in the organ. Accumula-tion of inflammatory cells may be a response to an ini-tial insult and/or a factor in driving BPH pathogenesis. Certainly, inflammation can limit the efficacy of existing medical therapies in these patients. We previously showed that a pattern of gene expression in BPH tis-sues from patients who had progressed to indication-specific surgery was consistent with the changes seen in AI diseases. Recently, we demonstrated that patients with AI disease have an approximately 50% increase in BPH prevalence compared to patients without AI dis-ease. Treatment of AI disease patients, specifically with TNF-antagonists, reduces BPH incidence back to, or in some diseases, below, the baseline population BPH di-agnosis rate. Treatment of AI disease patients with the broad spectrum anti-inflammatory methotrexate did not elicit this reduction in diagnoses. Systemic treat-ment with TNF antagonists reduces epithelial prolifera-tion and macrophage accumulation in the prostate tis-sues from two mouse models of prostatic hyperplasia as well as human patients. These studies suggest that TNF is a potential therapeutic target in BPH patients.
Keywords	benign prostatic hyperplasia ; inflammation ; autoimmune disease ; tumor necrosis factor ; therapy ; Medicine ; R ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Shared Science Publishers OG
Document type	Article ; Online
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Article ; Online: Fibroblast heterogeneity in prostate carcinogenesis.

ChallaSivaKanaka, Sathyavathi / Vickman, Renee E / Kakarla, Mamatha / Hayward, Simon W / Franco, Omar E

Cancer letters

2021 Volume 525, Page(s) 76–83

Abstract: Our understanding of stromal components, specifically cancer-associated fibroblasts (CAF), in prostate cancer (PCa), has evolved from considering these cells as inert bystanders to acknowledging their significance as players in prostate tumorigenesis. ... ...

Abstract	Our understanding of stromal components, specifically cancer-associated fibroblasts (CAF), in prostate cancer (PCa), has evolved from considering these cells as inert bystanders to acknowledging their significance as players in prostate tumorigenesis. CAF are multifaceted-they promote cancer cell growth, migration and remodel the tumor microenvironment. Although targeting CAF could be a promising strategy for PCa treatment, they incorporate a high but undefined degree of intrinsic cellular heterogeneity. The interaction between CAF subpopulations, with the normal and tumor epithelium and with other cell types is not yet characterized. Defining these interactions and the critical signaling nodes that support tumorigenesis will enable the development of novel strategies to control prostate cancer progression. Here we will discuss the origins, molecular and functional heterogeneity of CAF in PCa. We highlight the challenges associated with delineating CAF heterogeneity and discuss potential areas of research that would assist in expanding our knowledge of CAF and their role in PCa tumorigenesis.
MeSH term(s)	Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Carcinogenesis/genetics ; Cell Lineage/genetics ; Epithelium/metabolism ; Epithelium/pathology ; Genetic Heterogeneity ; Humans ; Male ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Stromal Cells/metabolism ; Stromal Cells/pathology ; Tumor Microenvironment/genetics
Language	English
Publishing date	2021-10-29
Publishing country	Ireland
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
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2021.10.028
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Article: Ephrin B Activate Src Family Kinases in Fibroblasts Inducing Stromal Remodeling in Prostate Cancer.

Kakarla, Mamatha / ChallaSivaKanaka, Sathyavathi / Dufficy, Mary F / Gil, Victoria / Filipovich, Yana / Vickman, Renee / Crawford, Susan E / Hayward, Simon W / Franco, Omar E

Cancers

2022 Volume 14, Issue 9

Abstract: Through stromal-epithelial interactions, carcinoma associated fibroblasts (CAF) play a critical role in tumor growth and progression. Activation of erythrophoyetin-producing human hepatocellular (Eph) receptors has been implicated in cancer. Eph receptor ...

Abstract	Through stromal-epithelial interactions, carcinoma associated fibroblasts (CAF) play a critical role in tumor growth and progression. Activation of erythrophoyetin-producing human hepatocellular (Eph) receptors has been implicated in cancer. Eph receptor interactions with Ephrin ligands lead to bidirectional signals in the recipient and effector cells. The consequences of continuous reverse Ephrin signaling activation in fibroblasts on prostate cancer (PCa) is unknown. When compared to benign prostate fibroblast, CAF displayed higher expression of Ephrin B1, B2, and B3 ligands (EFNB1, EFNB2, and EFNB3). In this study, we found that continuous activation of EFNB1 and EFNB3 in a benign human prostate stromal cell line (BHPrS1) increased the expression of CAF markers and induced a CAF phenotype. BHPrS1
Language	English
Publishing date	2022-05-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14092336
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Article ; Online: Shared Inherited Genetics of Benign Prostatic Hyperplasia and Prostate Cancer.

Glaser, Alexander / Shi, Zhuqing / Wei, Jun / Lanman, Nadia A / Ladson-Gary, Skylar / Vickman, Renee E / Franco, Omar E / Crawford, Susan E / Lilly Zheng, S / Hayward, Simon W / Isaacs, William B / Helfand, Brian T / Xu, Jianfeng

European urology open science

2022 Volume 43, Page(s) 54–61

Abstract: Background: The association between benign prostatic hyperplasia (BPH) and prostate cancer (PCa) remains controversial, largely due to a detection bias in traditional observational studies.: Objective: To assess the association between BPH and PCa ... ...

Abstract	Background: The association between benign prostatic hyperplasia (BPH) and prostate cancer (PCa) remains controversial, largely due to a detection bias in traditional observational studies. Objective: To assess the association between BPH and PCa using inherited single nucleotide polymorphisms (SNPs). Design setting and participants: The participants were White men from the population-based UK Biobank (UKB). Outcome measurements and statistical analysis: The association between BPH and PCa was tested for (1) phenotypic correlation using chi-square, (2) genetic correlation ( Results and limitations: Among 214 717 White men in the UKB, 24 623 (11%) and 14 311 (6.7%) had a diagnosis of BPH and PCa, respectively. Diagnoses of these two diseases were significantly correlated (χ Conclusions: BPH and PCa share common inherited genetics, which suggests that the phenotypic association of these two diseases in observational studies is not entirely caused by the detection bias. Patient summary: For the first time, we found that benign prostatic hyperplasia and prostate cancer are genetically related. This finding may have implications in disease etiology and risk stratification.
Language	English
Publishing date	2022-08-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3040546-4
ISSN	2666-1683 ; 2058-4881
ISSN (online)	2666-1683
ISSN	2058-4881
DOI	10.1016/j.euros.2022.07.004
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Article ; Online: Loss of ephrin B2 receptor (EPHB2) sets lipid rheostat by regulating proteins DGAT1 and ATGL inducing lipid droplet storage in prostate cancer cells.

Morales, Alejandro / Greenberg, Max / Nardi, Francesca / Gil, Victoria / Hayward, Simon W / Crawford, Susan E / Franco, Omar E

Laboratory investigation; a journal of technical methods and pathology

2021 Volume 101, Issue 7, Page(s) 921–934

Abstract: Lipid droplet (LD) accumulation in cancer results from aberrant metabolic reprograming due to increased lipid uptake, diminished lipolysis and/or de novo lipid synthesis. Initially implicated in storage and lipid trafficking in adipocytes, LDs are more ... ...

Abstract	Lipid droplet (LD) accumulation in cancer results from aberrant metabolic reprograming due to increased lipid uptake, diminished lipolysis and/or de novo lipid synthesis. Initially implicated in storage and lipid trafficking in adipocytes, LDs are more recently recognized to fuel key functions associated with carcinogenesis and progression of several cancers, including prostate cancer (PCa). However, the mechanisms controlling LD accumulation in cancer are largely unknown. EPHB2, a tyrosine kinase (TKR) ephrin receptor has been proposed to have tumor suppressor functions in PCa, although the mechanisms responsible for these effects are unclear. Given that dysregulation in TRK signaling can result in glutaminolysis we postulated that EPHB2 might have potential effects on lipid metabolism. Knockdown strategies for EPHB2 were performed in prostate cancer cells to analyze the impact on the net lipid balance, proliferation, triacylglycerol-regulating proteins, effect on LD biogenesis, and intracellular localization of LDs. We found that EPHB2 protein expression in a panel of human-derived prostate cancer cell lines was inversely associated with in vivo cell aggressiveness. EPHB2 silencing increased the proliferation of prostate cancer cells and concurrently induced de novo LD accumulation in both cytoplasmic and nuclear compartments as well as a "shift" on LD size distribution in newly formed lipid-rich organelles. Lipid challenge using oleic acid exacerbated the effects on the LD phenotype. Loss of EPHB2 directly regulated key proteins involved in maintaining lipid homeostasis including, increasing lipogenic DGAT1, DGAT2 and PLIN2 and decreasing lipolytic ATGL and PEDF. A DGAT1-specific inhibitor abrogated LD accumulation and proliferative effects induced by EPHB2 loss. In conclusion, we highlight a new anti-tumor function of EPHB2 in lipid metabolism through regulation of DGAT1 and ATGL in prostate cancer. Blockade of DGAT1 in EPHB2-deficient tumors appears to be effective in restoring the lipid balance and reducing tumor growth.
MeSH term(s)	Cell Line, Tumor ; Diacylglycerol O-Acyltransferase/metabolism ; Humans ; Lipase/metabolism ; Lipid Droplets/metabolism ; Lipid Metabolism/physiology ; Male ; Prostatic Neoplasms/metabolism ; Receptor, EphB2/genetics ; Receptor, EphB2/metabolism
Chemical Substances	DGAT1 protein, human (EC 2.3.1.20) ; Diacylglycerol O-Acyltransferase (EC 2.3.1.20) ; EPHB2 protein, human (EC 2.7.10.1) ; Receptor, EphB2 (EC 2.7.10.1) ; Lipase (EC 3.1.1.3) ; PNPLA2 protein, human (EC 3.1.1.3)
Language	English
Publishing date	2021-04-06
Publishing country	United States
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.
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1038/s41374-021-00583-9
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Article: The CINs of Polo-Like Kinase 1 in Cancer.

Cunningham, Chelsea E / MacAuley, Mackenzie J / Vizeacoumar, Frederick S / Abuhussein, Omar / Freywald, Andrew / Vizeacoumar, Franco J

Cancers

2020 Volume 12, Issue 10

Abstract: Polo-like kinase 1 (PLK1) is overexpressed near ubiquitously across all cancer types and dysregulation of this enzyme is closely tied to increased chromosomal instability and tumor heterogeneity. PLK1 is a mitotic kinase with a critical role in ... ...

Abstract	Polo-like kinase 1 (PLK1) is overexpressed near ubiquitously across all cancer types and dysregulation of this enzyme is closely tied to increased chromosomal instability and tumor heterogeneity. PLK1 is a mitotic kinase with a critical role in maintaining chromosomal integrity through its function in processes ranging from the mitotic checkpoint, centrosome biogenesis, bipolar spindle formation, chromosome segregation, DNA replication licensing, DNA damage repair, and cytokinesis. The relation between dysregulated PLK1 and chromosomal instability (CIN) makes it an attractive target for cancer therapy. However, clinical trials with PLK1 inhibitors as cancer drugs have generally displayed poor responses or adverse side-effects. This is in part because targeting CIN regulators, including PLK1, can elevate CIN to lethal levels in normal cells, affecting normal physiology. Nevertheless, aiming at related genetic interactions, such as synthetic dosage lethal (SDL) interactions of PLK1 instead of PLK1 itself, can help to avoid the detrimental side effects associated with increased levels of CIN. Since PLK1 overexpression contributes to tumor heterogeneity, targeting SDL interactions may also provide an effective strategy to suppressing this malignant phenotype in a personalized fashion.
Language	English
Publishing date	2020-10-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12102953
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Article ; Online: DGAT1 Inhibitor Suppresses Prostate Tumor Growth and Migration by Regulating Intracellular Lipids and Non-Centrosomal MTOC Protein GM130.

Nardi, Francesca / Franco, Omar E / Fitchev, Philip / Morales, Alejandro / Vickman, Renee E / Hayward, Simon W / Crawford, Susan E

Scientific reports

2019 Volume 9, Issue 1, Page(s) 3035

Abstract: Acyl-CoA:diacylglycerol acyltransferase I (DGAT1) is a key enzyme in lipogenesis which is increased in metabolically active cells to meet nutrient requirements. DGAT1 has been recognized as an anti-obesity target; however, its role in the tumor ... ...

Abstract	Acyl-CoA:diacylglycerol acyltransferase I (DGAT1) is a key enzyme in lipogenesis which is increased in metabolically active cells to meet nutrient requirements. DGAT1 has been recognized as an anti-obesity target; however, its role in the tumor microenvironment remains unclear. We postulated that, in prostate cancer (PCa) cells, augmented lipogenesis and growth are due to increased DGAT1 expression leading to microtubule-organizing center (MTOC) amplification. Thus, therapeutic targeting of DGAT1 potentially has tumor suppressive activity. We tested whether blocking DGAT1 in PCa cells altered MTOC and lipid signaling. Western blot and immunofluorescence were performed for MTOC and triglyceride mediators. Treatment with a DGAT1 inhibitor was evaluated. We found a stepwise increase in DGAT1 protein levels when comparing normal prostate epithelial cells to PCa cells, LNCaP and PC-3. Lipid droplets, MTOCs, and microtubule-regulating proteins were reduced in tumor cells treated with a DGAT1 inhibitor. Depletion of the non-centrosomal MTOC protein GM130 reduced PCa cell proliferation and migration. Inhibition of DGAT1 reduced tumor growth both in vitro and in vivo, and a negative feedback loop was discovered between DGAT1, PEDF, and GM130. These data identify DGAT1 as a promising new target for suppressing PCa growth by regulating GM130, MTOC number and disrupting microtubule integrity.
MeSH term(s)	Autoantigens/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Movement/physiology ; Cell Proliferation/physiology ; Diacylglycerol O-Acyltransferase/metabolism ; Epithelial Cells/metabolism ; Eye Proteins/metabolism ; Humans ; Lipid Droplets/metabolism ; Lipids ; Lipogenesis/physiology ; Male ; Membrane Proteins/metabolism ; Microtubule-Organizing Center/metabolism ; Microtubules/metabolism ; Nerve Growth Factors/metabolism ; PC-3 Cells ; Prostate/metabolism ; Prostatic Neoplasms/metabolism ; Serpins/metabolism
Chemical Substances	Autoantigens ; Eye Proteins ; Golgin subfamily A member 2 ; Lipids ; Membrane Proteins ; Nerve Growth Factors ; Serpins ; pigment epithelium-derived factor ; DGAT1 protein, human (EC 2.3.1.20) ; Diacylglycerol O-Acyltransferase (EC 2.3.1.20)
Language	English
Publishing date	2019-02-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-39537-z
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Article ; Online: Hyperglycemia and T Cell infiltration are associated with stromal and epithelial prostatic hyperplasia in the nonobese diabetic mouse.

Aaron-Brooks, LaTayia M / Sasaki, Takeshi / Vickman, Renee E / Wei, Lin / Franco, Omar E / Ji, Yuan / Crawford, Susan E / Hayward, Simon W

The Prostate

2019 Volume 79, Issue 9, Page(s) 980–993

Abstract: Background: Prostatic inflammation and various proinflammatory systemic comorbidities, such as diabetes and obesity are associated with human benign prostatic hyperplasia (BPH). There is a paucity of in vivo models reflecting specific aspects of BPH ... ...

Abstract	Background: Prostatic inflammation and various proinflammatory systemic comorbidities, such as diabetes and obesity are associated with human benign prostatic hyperplasia (BPH). There is a paucity of in vivo models reflecting specific aspects of BPH pathogenesis. Our aim was to investigate the nonobese diabetic (NOD) mouse as a potential model for subsequent intervention studies. Materials and methods: We used the NOD mouse, a model of autoimmune inflammation leading to type 1 diabetes to examine the effects of systemic inflammation and diabetes on the prostate. We assessed changes in prostatic histology, infiltrating leukocytes, and gene expression associated with aging and diabetic status. Results: Both stromal expansion and epithelial hyperplasia were observed in the prostates. Regardless of diabetic status, the degree of prostatic hyperplasia varied. Local inflammation was associated with a more severe prostatic phenotype in both diabetic and nondiabetic mice. Testicular atrophy was noted in diabetic mice, but prostate glands showed persistent focal cell proliferation. In addition, a prostatic intraepithelial neoplasia (PIN)-like phenotype was seen in several diabetic animals with an associated increase in c-Myc and MMP-2 expression. To examine changes in gene and cytokine expression we performed microarray and cytokine array analysis comparing the prostates of diabetic and nondiabetic animals. Microarray analysis revealed several differentially expressed genes including CCL3, CCL12, and TNFS10. Cytokine array analysis revealed increased expression of cytokines and proteases such as LDLR, IL28 A/B, and MMP-2 in diabetic mice. Conclusion: Overall, NOD mice provide a model to examine the effects of hyperglycemia and chronic inflammation on the prostate, demonstrating relevance to some of the mechanisms present underlying BPH and potentially the initiation of prostate cancer.
MeSH term(s)	Animals ; Cytokines/immunology ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/immunology ; Diabetes Mellitus, Experimental/pathology ; Epithelial Cells/immunology ; Epithelial Cells/pathology ; Hyperglycemia/immunology ; Hyperglycemia/pathology ; Male ; Mice ; Mice, Inbred NOD ; Prostatic Hyperplasia/blood ; Prostatic Hyperplasia/immunology ; Prostatic Hyperplasia/pathology ; Prostatic Intraepithelial Neoplasia/blood ; Prostatic Intraepithelial Neoplasia/immunology ; Prostatic Intraepithelial Neoplasia/pathology ; Prostatic Neoplasms/blood ; Prostatic Neoplasms/immunology ; Prostatic Neoplasms/pathology ; Stromal Cells/immunology ; Stromal Cells/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology ; Testis/pathology
Chemical Substances	Cytokines
Language	English
Publishing date	2019-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604707-5
ISSN	1097-0045 ; 0270-4137
ISSN (online)	1097-0045
ISSN	0270-4137
DOI	10.1002/pros.23809
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