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Article: Hedgehog in prostate cancer explained.

Buttyan, Ralph / Li, Na / Massah, Shabnam

Oncoscience

2018 Volume 5, Issue 3-4, Page(s) 67–68

Language	English
Publishing date	2018-04-29
Publishing country	United States
Document type	Editorial
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.405
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Article ; Online: Correction: Implications of PI3K/AKT inhibition on REST protein stability and neuroendocrine phenotype acquisition in prostate cancer cells.

Chen, Ruiqi / Li, Yinan / Buttyan, Ralph / Dong, Xuesen

Oncotarget

2018 Volume 9, Issue 51, Page(s) 29842

Abstract: This corrects the article DOI: 10.18632/oncotarget.19386.]. ...

Abstract	[This corrects the article DOI: 10.18632/oncotarget.19386.].
Language	English
Publishing date	2018-07-03
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.25759
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Article ; Online: Erythropoietin promotes functional recovery via anti-apoptotic mechanisms in mouse unilateral ureteral obstruction.

Park, Elliya / Cox, Michael / Scotland, Kymora / Buttyan, Ralph / Lange, Dirk

Cell stress & chaperones

2020 Volume 25, Issue 2, Page(s) 245–251

Abstract: The purpose of the work was to investigate mechanisms of erythropoietin-induced protection and accelerated recovery of kidneys and ureters from obstructive injury. Unilateral ureteral obstruction was established for 24, 48, and 72 h in C57BL/6 mice using ...

Abstract	The purpose of the work was to investigate mechanisms of erythropoietin-induced protection and accelerated recovery of kidneys and ureters from obstructive injury. Unilateral ureteral obstruction was established for 24, 48, and 72 h in C57BL/6 mice using a non-traumatic micro-clip followed by the microscopic quantification of ureteral peristalsis pre- and post-obstruction. Expression of erythropoietin, erythropoietin receptor, β-common receptor, and downstream apoptosis-related markers was assessed by RT-PCR and immunohistochemistry in ureters and kidneys and compared to the respective organs on the contralateral side within each animal. Expression of genes in kidneys and ureters from mice treated with 20 IU of erythropoietin daily for 72 h prior to obstruction was compared to that of untreated mice following obstruction. Apoptosis in ureteral tissues after 72-h obstruction was assessed via TUNEL assay. Ureteral obstruction increased apoptosis in affected ureters, with peristaltic function halted following all periods of obstruction. Erythropoietin treatment suppressed apoptosis in obstructed tissues and increased the percentage of mice retaining ureteral function immediately following obstruction reversal. Erythropoietin, erythropoietin receptor, Bcl-2, and Bcl-xl mRNA expression were down-regulated, while phospho-Nf-ĸb p65 was up-regulated in ureteral epithelia following obstruction. Erythropoietin treatment induced anti-apoptotic signaling via down-regulated Bax mRNA expression and abrogated phospho-Nf-ĸb p65. Erythropoietin-induced protection of ureteral function and accelerated recovery post-obstruction removal is mediated via anti-apoptotic mechanisms. Ureteral function is disrupted even following obstruction removal, negatively affecting renal function due to delayed recovery. Thus, our results represent a potential target for the development of safe therapeutic agents aimed at improving functional recovery from obstructive injury.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Epoetin Alfa/administration & dosage ; Epoetin Alfa/pharmacology ; Female ; Kidney/drug effects ; Kidney/injuries ; Mice ; Mice, Inbred C57BL ; Protective Agents/administration & dosage ; Protective Agents/pharmacology ; Recovery of Function ; Ureter/drug effects ; Ureter/injuries ; Ureteral Obstruction/drug therapy
Chemical Substances	Protective Agents ; Epoetin Alfa (64FS3BFH5W)
Language	English
Publishing date	2020-01-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1362749-1
ISSN	1466-1268 ; 1355-8145
ISSN (online)	1466-1268
ISSN	1355-8145
DOI	10.1007/s12192-020-01067-3
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Zs.A 4797: Show issues

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Article ; Online: Implications of PI3K/AKT inhibition on REST protein stability and neuroendocrine phenotype acquisition in prostate cancer cells.

Chen, Ruiqi / Li, Yinan / Buttyan, Ralph / Dong, Xuesen

Oncotarget

2017 Volume 8, Issue 49, Page(s) 84863–84876

Abstract: Treatment-induced neuroendocrine prostate cancer (t-NEPC) is an aggressive subtype of prostate cancer (PCa) that arises as a consequence of rigorous androgen receptor (AR) pathway inhibition (ARPI) therapies. While the PI3K/AKT pathway has been ... ...

Abstract	Treatment-induced neuroendocrine prostate cancer (t-NEPC) is an aggressive subtype of prostate cancer (PCa) that arises as a consequence of rigorous androgen receptor (AR) pathway inhibition (ARPI) therapies. While the PI3K/AKT pathway has been investigated as a co-therapeutic target with ARPI for advanced PCa, whether this strategy can prevent tumor progression to t-NEPC remains unknown. Here, we report that PI3K/AKT inhibition alone reduces RE-1 silencing transcription factor (REST) protein expression and induces multiple NE markers in PCa cells. The loss of REST by PI3K/AKT inhibition is through protein degradation mediated by the E3-ubiquitin ligase β-TRCP and REST phosphorylations at the S1024, S1027, and S1030 sites. Since AR inhibition can also deplete REST, the combinational inhibition of PI3K/AKT and AR further aggravated REST protein reduction. We profiled the transcriptomes of AKT and AR inhibitions in the LNCaP cells. The Gene Set Enrichment Analysis (GSEA) showed that these transcriptomes are highly correlated with the REST-regulated gene signature. Co-targeting AKT and AR resulted in a higher correlation comparing to those of single treatment. Comparing these transcriptomes to the t-NEPC gene signature in patients by GSEA, we observed that adding AKT inhibition to AR blockade enhanced the expression of neurogenesis-related genes and resulted in a stronger and broader upregulation of REST-regulated genes specific to t-NEPC. These results indicate that AKT pathway inhibition can induce neuroendocrine differentiation of PCa cells
Language	English
Publishing date	2017-07-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.19386
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Article ; Online: Semaphorin 3C promotes de novo steroidogenesis in prostate cancer cells.

Yenki, Parvin / Bhasin, Satyam / Liu, Liang / Nabavi, Noushin / Cheng, Chi Wing / Tam, Kevin J / Peacock, James W / Adomat, Hans H / Tombe, Tabitha / Fazli, Ladan / Ivanova, Larissa / Dusek, Christopher / Khosravi, Shahram / Guns, Emma S Tomlinson / Wang, Yuzhuo / Buttyan, Ralph / Gleave, Martin E / Ong, Christopher J

Endocrine-related cancer

2023 Volume 30, Issue 12

Abstract: Intratumoral androgen biosynthesis contributes to castration-resistant prostate cancer progression in patients treated with androgen deprivation therapy. The molecular mechanisms by which castration-resistant prostate cancer acquires the capacity for ... ...

Abstract	Intratumoral androgen biosynthesis contributes to castration-resistant prostate cancer progression in patients treated with androgen deprivation therapy. The molecular mechanisms by which castration-resistant prostate cancer acquires the capacity for androgen biosynthesis to bypass androgen deprivation therapy are not entirely known. Here, we show that semaphorin 3C, a secreted signaling protein that is highly expressed in castration-resistant prostate cancer, can promote steroidogenesis by altering the expression profile of key steroidogenic enzymes. Semaphorin 3C not only upregulates enzymes required for androgen synthesis from dehydroepiandrosterone or de novo from cholesterol but also simultaneously downregulates enzymes involved in the androgen inactivation pathway. These changes in gene expression correlate with increased production of androgens induced by semaphorin 3C in prostate cancer model cells. Moreover, semaphorin 3C upregulates androgen synthesis in LNCaP cell-derived xenograft tumors, likely contributing to the enhanced in vivo tumor growth rate post castration. Furthermore, semaphorin 3C activates sterol regulatory element-binding protein, a transcription factor that upregulates enzymes involved in the synthesis of cholesterol, a sole precursor for de novo steroidogenesis. The ability of semaphorin 3C to promote intratumoral androgen synthesis may be a key mechanism contributing to the reactivation of the androgen receptor pathway in castration-resistant prostate cancer, conferring continued growth under androgen deprivation therapy. These findings identify semaphorin 3C as a potential therapeutic target for suppressing intratumoral steroidogenesis.
MeSH term(s)	Male ; Humans ; Androgens/metabolism ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Androgen Antagonists ; Receptors, Androgen/metabolism ; Cholesterol/metabolism ; Semaphorins/genetics ; Semaphorins/metabolism ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic
Chemical Substances	Androgens ; Androgen Antagonists ; Receptors, Androgen ; Cholesterol (97C5T2UQ7J) ; Semaphorins
Language	English
Publishing date	2023-11-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1530/ERC-23-0010
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Zs.A 4192: Show issues

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Article ; Online: Gli activation by the estrogen receptor in breast cancer cells: Regulation of cancer cell growth by Gli3.

Massah, Shabnam / Foo, Jane / Li, Na / Truong, Sarah / Nouri, Mannan / Xie, Lishi / Prins, Gail S / Buttyan, Ralph

Molecular and cellular endocrinology

2020 Volume 522, Page(s) 111136

Abstract: Background: Gli is an oncogenic transcription factor family thought to be involved in breast cancer (BrCa) cell growth. Gli activity is regulated by a post-translational proteolytic process that is suppressed by Hedgehog signaling. In prostate cancer ... ...

Abstract	Background: Gli is an oncogenic transcription factor family thought to be involved in breast cancer (BrCa) cell growth. Gli activity is regulated by a post-translational proteolytic process that is suppressed by Hedgehog signaling. In prostate cancer cells, however, Gli activation is mediated by an interaction of active androgen receptor proteins with Gli3 that stabilizes Gli3 in its un-proteolyzed form. Here we show that the estrogen receptor (ER), ERα, also binds Gli3 and activates Gli in BrCa cells. Moreover, we show that ER + BrCa cells are dependent on Gli3 for cancer cell growth. Methods: Transfection with Gli-luciferase reporter was used to report Gli activity in 293FT or BrCa cells (MCF7, T47D, MDA-MB-453) with or without steroid ligands. Co-immunoprecipitation and proximity ligation were used to show association of Gli3 with ERα. Gli3 stability was determined by western blots of BrCa cell extracts. ERα knockdown or destabilization (by fulvestrant) was used to assess how loss of ERα affects estradiol-induced Gli reporter activity, formation of intranuclear ERα-Gli3 complexes and Gli3 stability. Expression of Gli1 and/or other endogenous Gli-target genes in BrCa cells were measured by qPCR in the presence or absence of estradiol. Gli3 knockdown was assessed for effects on BrCa cell growth using the Cyquant assay. Results: ERα co-transfection increased Gli reporter activity in 293FT cells that was further increased by estradiol. Gli3 co-precipitated in ERα immunoprecipitates. Acute (2 h) estradiol increased Gli reporter activity and the formation of intranuclear ERα-Gli3 complexes in ER + BrCa cells but more chronic estradiol (48 h) reduced ERα-Gli complexes commensurate with reduced ERα levels. Gli3 stability and endogenous activity was only increased by more chronic estradiol treatment. Fulvestrant or ERα knockdown suppressed E2-induction of Gli activity, intranuclear ERα-Gli3 complexes and stabilization of Gli3. Gli3 knockdown significantly reduced the growth of BrCa cells. Conclusions: ERα interacts with Gli3 in BrCa cells and estradiol treatment leads to Gli3 stabilization and increased expression of Gli-target genes. Furthermore, we found tthat Gli3 is necessary for BrCa cell growth. These results support the idea that the ERα-Gli interaction and Gli3 may be novel targets for effective control of BrCa growth.
MeSH term(s)	Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cell Proliferation/drug effects ; Estradiol/pharmacology ; Female ; HEK293 Cells ; Humans ; Protein Stability/drug effects ; Receptors, Estrogen/metabolism ; Zinc Finger Protein Gli3/metabolism
Chemical Substances	Receptors, Estrogen ; Zinc Finger Protein Gli3 ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2020-12-25
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111136
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Zs.A 1127: Show issues

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Article: Gli activation by the estrogen receptor in breast cancer cells: Regulation of cancer cell growth by Gli3

Massah, Shabnam / Foo, Jane / Li, Na / Truong, Sarah / Nouri, Mannan / Xie, Lishi / Prins, Gail S / Buttyan, Ralph

Molecular and cellular endocrinology. 2021 Feb. 15, v. 522

2021

Abstract: Gli is an oncogenic transcription factor family thought to be involved in breast cancer (BrCa) cell growth. Gli activity is regulated by a post-translational proteolytic process that is suppressed by Hedgehog signaling. In prostate cancer cells, however, ...

Abstract	Gli is an oncogenic transcription factor family thought to be involved in breast cancer (BrCa) cell growth. Gli activity is regulated by a post-translational proteolytic process that is suppressed by Hedgehog signaling. In prostate cancer cells, however, Gli activation is mediated by an interaction of active androgen receptor proteins with Gli3 that stabilizes Gli3 in its un-proteolyzed form. Here we show that the estrogen receptor (ER), ERα, also binds Gli3 and activates Gli in BrCa cells. Moreover, we show that ER + BrCa cells are dependent on Gli3 for cancer cell growth.Transfection with Gli-luciferase reporter was used to report Gli activity in 293FT or BrCa cells (MCF7, T47D, MDA-MB-453) with or without steroid ligands. Co-immunoprecipitation and proximity ligation were used to show association of Gli3 with ERα. Gli3 stability was determined by western blots of BrCa cell extracts. ERα knockdown or destabilization (by fulvestrant) was used to assess how loss of ERα affects estradiol-induced Gli reporter activity, formation of intranuclear ERα-Gli3 complexes and Gli3 stability. Expression of Gli1 and/or other endogenous Gli-target genes in BrCa cells were measured by qPCR in the presence or absence of estradiol. Gli3 knockdown was assessed for effects on BrCa cell growth using the Cyquant assay.ERα co-transfection increased Gli reporter activity in 293FT cells that was further increased by estradiol. Gli3 co-precipitated in ERα immunoprecipitates. Acute (2 h) estradiol increased Gli reporter activity and the formation of intranuclear ERα-Gli3 complexes in ER + BrCa cells but more chronic estradiol (48 h) reduced ERα-Gli complexes commensurate with reduced ERα levels. Gli3 stability and endogenous activity was only increased by more chronic estradiol treatment. Fulvestrant or ERα knockdown suppressed E2-induction of Gli activity, intranuclear ERα-Gli3 complexes and stabilization of Gli3. Gli3 knockdown significantly reduced the growth of BrCa cells.ERα interacts with Gli3 in BrCa cells and estradiol treatment leads to Gli3 stabilization and increased expression of Gli-target genes. Furthermore, we found tthat Gli3 is necessary for BrCa cell growth. These results support the idea that the ERα-Gli interaction and Gli3 may be novel targets for effective control of BrCa growth.
Keywords	Western blotting ; androgen receptors ; breast neoplasms ; cell growth ; coprecipitation ; estradiol ; estrogen receptors ; extracts ; genes ; ligands ; neoplasm cells ; precipitin tests ; prostatic neoplasms ; proteolysis
Language	English
Dates of publication	2021-0215
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-light
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2020.111136
Database	NAL-Catalogue (AGRICOLA)

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Article: Editorial comment on: Hedgehog signalling in androgen independent prostate cancer.

Chen, Mengqian / Buttyan, Ralph

European urology

2008 Volume 54, Issue 6, Page(s) 1341–1343

MeSH term(s)	Androgens/physiology ; Hedgehog Proteins/physiology ; Humans ; Male ; Prostatic Neoplasms/etiology ; Signal Transduction
Chemical Substances	Androgens ; Hedgehog Proteins
Language	English
Publishing date	2008-12
Publishing country	Switzerland
Document type	Comment ; Editorial
ZDB-ID	193790-x
ISSN	1421-993X ; 0302-2838
ISSN (online)	1421-993X
ISSN	0302-2838
DOI	10.1016/j.eururo.2008.01.071
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Zs.A 1247: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 294: Show issues

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Article: Molecularly targeted therapies for renal cell cancer: TRAIL research advances.

Buttyan, Ralph / Mian, Badar M

The Journal of urology

2007 Volume 177, Issue 5, Page(s) 1606

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Apoptosis/drug effects ; Carcinoma, Renal Cell/drug therapy ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Humans ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Receptors, Vascular Endothelial Growth Factor/drug effects ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2007-05
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	3176-8
ISSN	1527-3792 ; 0022-5347
ISSN (online)	1527-3792
ISSN	0022-5347
DOI	10.1016/j.juro.2007.01.109
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Ui VI Zs.91: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 331: Show issues

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Article ; Online: Non-canonical activation of hedgehog in prostate cancer cells mediated by the interaction of transcriptionally active androgen receptor proteins with Gli3.

Li, Na / Truong, Sarah / Nouri, Mannan / Moore, Jackson / Al Nakouzi, Nader / Lubik, Amy Anne / Buttyan, Ralph

Oncogene

2018 Volume 37, Issue 17, Page(s) 2313–2325

Abstract: Hedgehog (Hh) is an oncogenic signaling pathway that regulates the activity of Gli transcription factors. Canonical Hh is a Smoothened- (Smo-) driven process that alters the post-translational processing of Gli2/Gli3 proteins. Though evidence supports a ... ...

Abstract	Hedgehog (Hh) is an oncogenic signaling pathway that regulates the activity of Gli transcription factors. Canonical Hh is a Smoothened- (Smo-) driven process that alters the post-translational processing of Gli2/Gli3 proteins. Though evidence supports a role for Gli action in prostate cancer (PCa) cell growth and progression, there is little indication that Smo is involved. Here we describe a non-canonical means for activation of Gli transcription in PCa cells mediated by the binding of transcriptionally-active androgen receptors (ARs) to Gli3. Androgens stimulated reporter expression from a Gli-dependent promoter in a variety of AR + PCa cells and this activity was suppressed by an anti-androgen, Enz, or by AR knockdown. Androgens also upregulated expression of endogenous Gli-dependent genes. This activity was associated with increased intranuclear binding of Gli3 to AR that was antagonized by Enz. Fine mapping of the AR binding domain on Gli2 showed that AR recognizes the Gli protein processing domain (PPD) in the C-terminus. Mutations in the arginine-/serine repeat elements of the Gli2 PPD involved in phosphorylation and ubiquitinylation blocked the binding to AR. β-TrCP, a ubiquitin ligase that recognizes the Gli PPD, competed with AR for binding to this site. AR binding to Gli3 suppressed its proteolytic processing to the Gli3 repressor form (Gli3R) whereas AR knockdown increased Gli3R. Both full-length and truncated ARs were able to activate Gli transcription. Finally, we found that an ARbinding decoy polypeptide derived from the Gli2 C-terminus can compete with Gli3 for binding to AR. Exogenous overexpression of this decoy suppressed Gli transcriptional activity in PCa cells. Collectively, this work identifies a novel pathway for non-canonical activation of Hh signaling in PCa cells and identifies a means for interference that may have clinical relevance for PCa patients.
MeSH term(s)	Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Hedgehog Proteins/genetics ; Humans ; Male ; Nerve Tissue Proteins/metabolism ; Promoter Regions, Genetic ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Binding ; Receptors, Androgen/metabolism ; Signal Transduction/physiology ; Transcription Factors/metabolism ; Transcriptional Activation ; Zinc Finger Protein Gli3/metabolism
Chemical Substances	AR protein, human ; GLI3 protein, human ; Hedgehog Proteins ; Nerve Tissue Proteins ; Receptors, Androgen ; Transcription Factors ; Zinc Finger Protein Gli3
Language	English
Publishing date	2018-02-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-017-0098-7
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