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Article ; Online: Dicer protein levels elevated by mild hyperthermia promote a pro-survival phenotype.

Devasthanam, Anand S / Tomasi, Thomas B

2017 Volume 8, Issue 40, Page(s) 67001–67016

Abstract: Cellular exposure to mild stress (39.5°C - 41.5°C) induces thermotolerance, rendering cells resistant to a subsequent heat shock (>42°C) insult. We found that mild hyperthermia at 39.5°C leads to elevations in dicer, a protein well-known for its role in ... ...

Abstract	Cellular exposure to mild stress (39.5°C - 41.5°C) induces thermotolerance, rendering cells resistant to a subsequent heat shock (>42°C) insult. We found that mild hyperthermia at 39.5°C leads to elevations in dicer, a protein well-known for its role in microRNA processing and for its role in cellular stress responses. However, whether elevated dicer protein levels play a role in sustaining a thermotolerant phenotype has, to our knowledge, not been reported. Here we demonstrate that elevated dicer protein is linked to a thermotolerant phenotype in the cervical carcinoma cell line HeLa and in murine embryonic fibroblasts (MEF), and demonstrate that dicer plays a role in mediating PKR and eIF2α phosphorylation. These findings suggest that dicer's role in thermotolerance may be to relay signals to key ER stress pathway components. Moreover, utilizing a MEF cell line defective in microRNA processing, we suggest that dicer's influence on PKR and eIF2α phosphorylation is likely distinct from its microRNA processing role. ATF4 and CHOP are well characterized stress response factors proximal to eIF2α. Evidence is presented that elevated dicer protein in thermotolerant cells differentially modulates ATF4 and CHOP levels to promote a pro-survival phenotype. This work contributes new information on dicer's role in cellular stress responses by defining a pro-survival phenotype in heat stress resistant cells which is sustained, at least in part, by elevated dicer protein levels. Our results suggest an ancillary role for dicer in the cellular stress pathways activated by mild hyperthermia that is likely distinct from its role in microRNA processing.
Language	English
Publishing date	2017-09-15
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.17433
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The epigenetic regulation of Dicer and microRNA biogenesis by Panobinostat.

Hoffend, Nicholas C / Magner, William J / Tomasi, Thomas B

Epigenetics

2017 Volume 12, Issue 2, Page(s) 105–112

Abstract: microRNAs (miRs) are small noncoding RNAs that regulate/fine tune many cellular protein networks by targeting mRNAs for either degradation or translational inhibition. Dicer, a type III endoribonuclease, is a critical component in miR biogenesis and is ... ...

Abstract	microRNAs (miRs) are small noncoding RNAs that regulate/fine tune many cellular protein networks by targeting mRNAs for either degradation or translational inhibition. Dicer, a type III endoribonuclease, is a critical component in miR biogenesis and is required for mature microRNA production. Abnormal Dicer expression occurs in numerous cancer types and correlates with poor patient prognosis. Recent reports have demonstrated that epigenetic agents, including histone deacetylase inhibitors (HDACi), may regulate Dicer and miR expression. HDACi are a class of epigenetic agents used to treat cancer, viral infections, and inflammatory disorders. However, little is known regarding the epigenetic regulation of miR biogenesis and function. We therefore investigated whether clinically successful HDACi modulated Dicer expression and found that Panobinostat, a clinically approved HDACi, enhanced Dicer expression via posttranscriptional mechanisms. Studies using proteasome inhibitors suggested that Panobinostat regulated the proteasomal degradation of Dicer. Further studies demonstrated that Panobinostat, despite increasing Dicer protein expression, decreased Dicer activity. This suggests that Dicer protein levels do not necessarily correlate with Dicer activity and mature miR levels. Taken together, we present evidence here that Panobinostat posttranscriptionally regulates Dicer/miR biogenesis and suggest Dicer as a potential therapeutic target in cancer.
MeSH term(s)	Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic/drug effects ; HeLa Cells ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Hydroxamic Acids/pharmacology ; Indoles/pharmacology ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Ribonuclease III/genetics ; Ribonuclease III/metabolism
Chemical Substances	Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Indoles ; MicroRNAs ; panobinostat (9647FM7Y3Z) ; Ribonuclease III (EC 3.1.26.3)
Language	English
Publishing date	2017-02
Publishing country	United States
Document type	Journal Article
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.1080/15592294.2016.1267886
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Book: The immune system of secretions

Tomasi, Thomas B.

(Prentice Hall Foundations of Immunology Series)

1976

Author's details	Thomas B. Tomasi
Series title	Prentice Hall Foundations of Immunology Series
Keywords	Immunsystem ; Sekretion
Subject	Secretion ; Körpereigene Abwehr ; Körpereigene Abwehrkräfte ; Körpereigenes Abwehrsystem ; Abwehrkräfte
Language	English
Size	XII, 161 S.
Publisher	Prentice Hall
Publishing place	Englewood Cliffs, NJ
Publishing country	United States
Document type	Book
HBZ-ID	HT010499643
ISBN	0-13-451609-5 ; 978-0-13-451609-7
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Dicer in immune cell development and function.

Devasthanam, Anand S / Tomasi, Thomas B

Immunological investigations

2013 Volume 43, Issue 2, Page(s) 182–195

Abstract: Dicer is an enzyme of the RNase III endoribonuclease family, which is crucial for RNA interference (RNAi) in eukaryotes. Dicer is a component of the protein machinery (the RNA Induced Silencing Complex [RISC]) which is involved in catalyzing the ... ...

Abstract	Dicer is an enzyme of the RNase III endoribonuclease family, which is crucial for RNA interference (RNAi) in eukaryotes. Dicer is a component of the protein machinery (the RNA Induced Silencing Complex [RISC]) which is involved in catalyzing the formation of mature microRNAs from their precursors in the process of microRNA biogenesis. RISC-associated microRNAs bind to specific sequences in the 3' untranslated region of cognate mRNAs largely through complementary base pairing, resulting in either translational inhibition and/or the degradation of a specific mRNA pool. MicroRNAs epigenetically regulate the cellular levels of receptors, transcription factors and signaling proteins that govern the developmental pathways and functions of multiple cellular processes. The pivotal role played by Dicer in microRNA formation has also piqued the interest of molecular immunologists who have sought to understand the biological relevance of microRNAs in the development and function of the immune system. Here, we review the major findings of these studies and provide an overview of the role of Dicer and microRNAs in immune cell development and function. Additionally, we highlight deficiencies in our knowledge and new research areas that may enhance our understanding of the role of Dicer and microRNAs in immunity.
MeSH term(s)	Animals ; Cell Differentiation ; Epigenesis, Genetic/immunology ; Gene Expression Regulation, Developmental ; Humans ; Immune System/embryology ; Immune System/growth & development ; Immunity, Cellular ; MicroRNAs/physiology ; RNA Interference ; Ribonuclease III/immunology
Chemical Substances	MicroRNAs ; Ribonuclease III (EC 3.1.26.3)
Language	English
Publishing date	2013-12-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	632565-8
ISSN	1532-4311 ; 0882-0139
ISSN (online)	1532-4311
ISSN	0882-0139
DOI	10.3109/08820139.2013.863557
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Zs.A 988: Show issues

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Article ; Online: The modulation of Dicer regulates tumor immunogenicity in melanoma.

Hoffend, Nicholas C / Magner, William J / Tomasi, Thomas B

Oncotarget

2016 Volume 7, Issue 30, Page(s) 47663–47673

Abstract: MicroRNAs (miRs) are small non-coding RNAs that regulate most cellular protein networks by targeting mRNAs for translational inhibition or degradation. Dicer, a type III endoribonuclease, is a critical component in microRNA biogenesis and is required for ...

Abstract	MicroRNAs (miRs) are small non-coding RNAs that regulate most cellular protein networks by targeting mRNAs for translational inhibition or degradation. Dicer, a type III endoribonuclease, is a critical component in microRNA biogenesis and is required for mature microRNA production. Abnormal Dicer expression occurs in numerous cancer types and correlates with poor patient prognosis. For example, increased Dicer expression in melanoma is associated with more aggressive tumors (higher tumor mitotic index and depth of invasion) and poor patient prognosis. However, the role that Dicer plays in melanoma development and immune evasion remains unclear. Here, we report on a newly discovered relationship between Dicer expression and tumor immunogenicity. To investigate Dicer's role in regulating melanoma immunogenicity, Dicer knockdown studies were performed. We found that B16F0-Dicer deficient cells exhibited decreased tumor growth compared to control cells and were capable of inducing anti-tumor immunity. The decrease in tumor growth was abrogated in immunodeficient NSG mice and was shown to be dependent upon CD8+ T cells. Dicer knockdown also induced a more responsive immune gene profile in melanoma cells. Further studies demonstrated that CD8+ T cells preferentially killed Dicer knockdown tumor cells compared to control cells. Taken together, we present evidence which links Dicer expression to tumor immunogenicity in melanoma.
Language	English
Publishing date	2016-07-26
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.10273
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Article ; Online: VSSP abrogates murine ovarian tumor-associated myeloid cell-driven immune suppression and induces M1 polarization in tumor-associated macrophages from ovarian cancer patients.

Khan, Anm Nazmul H / Emmons, Tiffany R / Magner, William J / Alqassim, Emad / Singel, Kelly L / Ricciuti, Jason / Eng, Kevin H / Odunsi, Kunle / Tomasi, Thomas B / Lee, Kelvin / Abrams, Scott I / Mesa, Circe / Segal, Brahm H

Cancer immunology, immunotherapy : CII

2022 Volume 71, Issue 10, Page(s) 2355–2369

Abstract: The ovarian tumor microenvironment (TME) is characterized by the accumulation of immunosuppressive tumor-associated macrophages (TAMs) and granulocytic cells. Very small size particles (VSSP), comprised of the ganglioside NAcGM3 and Neisseria ... ...

Abstract	The ovarian tumor microenvironment (TME) is characterized by the accumulation of immunosuppressive tumor-associated macrophages (TAMs) and granulocytic cells. Very small size particles (VSSP), comprised of the ganglioside NAcGM3 and Neisseria meningitidis derived outer membrane vesicles, is being developed as a nanoparticulated modulator of innate immunity. Prior studies have shown that VSSP enhanced antigen-specific cytotoxic T cell responses and reduced the suppressive phenotype of splenic granulocytic cells in tumor-bearing mice. Here, we hypothesized that intraperitoneal VSSP would modify myeloid cell accumulation and phenotypes in the ovarian TME and abrogate suppressor function of TAMs and tumor-associated granulocytic cells. In the ID8 syngeneic model of epithelial ovarian cancer, VSSP reduced peritoneal TAMs and induced M1-like polarization in TAMs. In addition, VSSP stimulated peritoneal inflammation characterized by increased granulocytes and monocytes, including inflammatory monocytic cells. VSSP treatment resulted in peritoneal TAMs and granulocytic cells being less suppressive of ex vivo stimulated CD8
MeSH term(s)	Animals ; Carcinoma, Ovarian Epithelial ; Cell Line, Tumor ; Female ; Humans ; Mice ; Mice, Inbred C57BL ; Myeloid Cells ; Ovarian Neoplasms ; Tumor Microenvironment ; Tumor-Associated Macrophages
Language	English
Publishing date	2022-02-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-022-03156-x
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Zs.A 1237: Show issues

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Article ; Online: Mild hyperthermia enhances the expression and induces oscillations in the Dicer protein.

Oshlag, Julian Z / Devasthanam, Anand S / Tomasi, Thomas B

International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group

2013 Volume 29, Issue 1, Page(s) 51–61

Abstract: Purpose: To investigate whether mild heat stress at 39.5°C altered Dicer protein and miRNA expression patterns in several cell types.: Methods: Multiple human and mouse cell types were cultured during the course of 9 h at temperatures from 37°C to 39. ...

Abstract	Purpose: To investigate whether mild heat stress at 39.5°C altered Dicer protein and miRNA expression patterns in several cell types. Methods: Multiple human and mouse cell types were cultured during the course of 9 h at temperatures from 37°C to 39.5°C. Dicer mRNA levels and microRNAs were quantified by TaqMan RT-qPCR assays and Dicer protein by western blotting. Results: Dicer protein was substantially elevated on western analysis in response to heat stress at 39.5°C in the absence of significant changes in Dicer mRNA by RT-qPCR. Conclusions: Heat-induced regulation of Dicer expression occurs primarily post- transcriptionally, and the expression levels of Dicer protein are increased and often oscillate in response to fever-range hyperthermia in multiple mouse and human cells. Our studies suggest a potential role for Dicer and microRNAs in the response to mild thermal stress. Additional studies on the mechanisms involved in the stress-induced oscillations of Dicer protein and microRNAs will be of interest.
MeSH term(s)	Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; HSP70 Heat-Shock Proteins/genetics ; HSP90 Heat-Shock Proteins/genetics ; Humans ; Hyperthermia, Induced ; Kidney/cytology ; Mice ; Mice, Inbred C57BL ; MicroRNAs/metabolism ; RNA, Messenger/metabolism ; Ribonuclease III/genetics ; Ribonuclease III/metabolism
Chemical Substances	HSP70 Heat-Shock Proteins ; HSP90 Heat-Shock Proteins ; MicroRNAs ; RNA, Messenger ; DICER1 protein, human (EC 3.1.26.3) ; Dicer1 protein, mouse (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2013-01-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	632526-9
ISSN	1464-5157 ; 0265-6736
ISSN (online)	1464-5157
ISSN	0265-6736
DOI	10.3109/02656736.2012.753471
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Zs.A 2051: Show issues

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Article: Spatial distribution of histone methylation during MHC class II expression.

Chou, Shiuh-Dih / Tomasi, Thomas B

Molecular immunology

2008 Volume 45, Issue 4, Page(s) 971–980

Abstract: ... of the B cell lines while the level remained low and unchanged despite active MHC class II expression ... transfection of a CIITA deficient B cell line restored the H3K79me2 to a level comparable to its cell of origin ...

Abstract	We have previously reported that Major Histocompatibility Complex (MHC) class II can be induced by histone deacetylase inhibitors (HDACi) in the absence of class II transactivator (CIITA). Here we characterized the histone modifications associated with the CIITA-dependent (IFN-gamma induced) and -independent (HDACi induced) MHC class II expression. We demonstrate that both IFN-gamma and HDACi induced MHC class II expression exhibited enhanced histone H3, H4 acetylation and H3K4me3 at the MHC class II promoter while H3K9me3 was decreased. In contrast, high levels of H3K36me3 were detected at exons 3 and 5 but not at the promoter or the locus control region (LCR). Interestingly, high levels of H3K79me2 were only detected at the promoter and exon 3 of the B cell lines while the level remained low and unchanged despite active MHC class II expression induced by either IFN-gamma or HDACi treatment. Constitutive expression of the CIITA protein by stable transfection of a CIITA deficient B cell line restored the H3K79me2 to a level comparable to its cell of origin. This data demonstrates that, although regulated by different pathways, both IFN-gamma and HDACi treatments resulted in similar patterns of histone modifications and that HDACi induce both histone methylation and acetylation. In addition, the different spatial distribution of the lysine methylation markers along the gene suggests that these modifications play a distinctive role during different phases of the transcription process.
MeSH term(s)	Acetylation ; Animals ; B-Lymphocytes/metabolism ; Cell Line ; Gene Expression Regulation ; Histocompatibility Antigens Class II/biosynthesis ; Histone Deacetylases/physiology ; Histones/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Interferon-gamma/pharmacology ; Lysine/metabolism ; Methylation ; Mice ; Nuclear Proteins/physiology ; Promoter Regions, Genetic ; Trans-Activators/physiology
Chemical Substances	Histocompatibility Antigens Class II ; Histones ; Hydroxamic Acids ; MHC class II transactivator protein ; Nuclear Proteins ; Trans-Activators ; trichostatin A (3X2S926L3Z) ; Interferon-gamma (82115-62-6) ; Histone Deacetylases (EC 3.5.1.98) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2008-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2007.07.039
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Zs.A 166: Show issues

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Article ; Online: Dicer is regulated by cellular stresses and interferons.

Wiesen, Jennifer L / Tomasi, Thomas B

Molecular immunology

2008 Volume 46, Issue 6, Page(s) 1222–1228

Abstract: The generation of microRNAs is dependent on the RNase III enzyme Dicer, the levels of which vary in different normal cells and in disease states. We demonstrate that Dicer protein expression in JAR trophoblast cells, and several other cell types, was ... ...

Abstract	The generation of microRNAs is dependent on the RNase III enzyme Dicer, the levels of which vary in different normal cells and in disease states. We demonstrate that Dicer protein expression in JAR trophoblast cells, and several other cell types, was inhibited by multiple stresses including reactive oxygen species, phorbol esters and the Ras oncogene. Additionally, double-stranded RNA and Type I interferons repress Dicer protein in contrast to IFN-gamma which induces Dicer. The effects of stresses and interferons are primarily post-transcriptional. The findings suggest that Dicer is a stress response component and identifies interferons as potentially important regulators of Dicer expression.
MeSH term(s)	Animals ; Cell Line ; Cell Line, Tumor ; Enzyme Activation ; Gene Expression Regulation, Enzymologic ; Histone Deacetylase Inhibitors ; Humans ; Hydroxamic Acids/pharmacology ; Interferon Type I/pharmacology ; Interferon Type I/physiology ; Interferon-gamma/pharmacology ; Interferon-gamma/physiology ; Mice ; MicroRNAs/metabolism ; Phorbol Esters/pharmacology ; Poly I-C/pharmacology ; Reactive Oxygen Species/metabolism ; Ribonuclease III/antagonists & inhibitors ; Ribonuclease III/biosynthesis ; Trophoblasts/metabolism ; ras Proteins/metabolism
Chemical Substances	Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Interferon Type I ; MicroRNAs ; Phorbol Esters ; Reactive Oxygen Species ; trichostatin A (3X2S926L3Z) ; Interferon-gamma (82115-62-6) ; Ribonuclease III (EC 3.1.26.3) ; ras Proteins (EC 3.6.5.2) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2008-12-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2008.11.012
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Zs.A 166: Show issues

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Article: The major histocompatibility complex class II transactivator is differentially regulated by interferon-gamma and transforming growth factor-beta in microglial cells.

Pazmany, Tamas / Tomasi, Thomas B

Journal of neuroimmunology

2006 Volume 172, Issue 1-2, Page(s) 18–26

Abstract: We evaluated the regulation of the major histocompatibility complex class II (MHC II) transactivator (CIITA) gene expression in two microglial cell lines, EOC2 and EOC20. We demonstrate that interferon-gamma (IFN-gamma) activates type III- and IV-CIITA ... ...

Abstract	We evaluated the regulation of the major histocompatibility complex class II (MHC II) transactivator (CIITA) gene expression in two microglial cell lines, EOC2 and EOC20. We demonstrate that interferon-gamma (IFN-gamma) activates type III- and IV-CIITA mRNA and high levels of MHC II in EOC20. However, in EOC2 cells only low levels of type IV-CIITA mRNA and MHC II are detectable following IFN-gamma treatment. Transforming growth factor-beta1 (TGF-beta1) inhibits both type III- and IV-CIITA expression in EOC20 cells while, in EOC2 cells TGF-beta1 enhances IFN-gamma induced pIV-CIITA expression. Trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, abrogates the TGF-beta1 mediated repression of the IFN-gamma induced CIITA in EOC20. Evidence is presented that the TG-interacting factor (TGIF), a co-repressor known to recruit HDACs, plays a role in determining the effects of TGF-beta1 on microglial cells.
MeSH term(s)	Animals ; Blotting, Western/methods ; Cell Differentiation/drug effects ; Cell Line ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cytosol/drug effects ; Cytosol/metabolism ; Dose-Response Relationship, Drug ; Drug Interactions ; Gene Expression/drug effects ; Gene Expression Regulation/drug effects ; Histocompatibility Antigens Class II/genetics ; Histocompatibility Antigens Class II/metabolism ; Hydroxamic Acids/pharmacology ; Interferon-gamma/pharmacology ; Mice ; Microglia/cytology ; Microglia/drug effects ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Protein Synthesis Inhibitors/pharmacology ; RNA, Messenger/biosynthesis ; Reverse Transcriptase Polymerase Chain Reaction/methods ; STAT Transcription Factors/metabolism ; Signal Transduction/drug effects ; Time Factors ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Transforming Growth Factor beta/pharmacology
Chemical Substances	Histocompatibility Antigens Class II ; Hydroxamic Acids ; MHC class II transactivator protein ; Nuclear Proteins ; Protein Synthesis Inhibitors ; RNA, Messenger ; STAT Transcription Factors ; Trans-Activators ; Transforming Growth Factor beta ; trichostatin A (3X2S926L3Z) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2006-03
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2005.10.009
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