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Article ; Online: Timing is everything: order of administration of 5-aza 2' deoxycytidine, trichostatin A and tamoxifen changes estrogen receptor mRNA expression and cell sensitivity.

Hostetter, Christine L / Licata, Lauren A / Keen, Judith Clancy

2009 Volume 275, Issue 2, Page(s) 178–184

Abstract: Restoration of estrogen receptor (ER) expression using epigenetic inhibitors re-establishes expression of the estrogen receptor (ER) and restores tamoxifen sensitivity in ER negative breast cancer cells. We tested if order of administration of the DNMT ( ... ...

Abstract	Restoration of estrogen receptor (ER) expression using epigenetic inhibitors re-establishes expression of the estrogen receptor (ER) and restores tamoxifen sensitivity in ER negative breast cancer cells. We tested if order of administration of the DNMT (5-aza 2' deoxycytidine/AZA) or HDAC (trichostatin A/TSA) inhibitors and tamoxifen affected ER re-expression and tamoxifen sensitivity. Treatment with AZA followed by co-administration of TSA plus tamoxifen resulted in the greatest ER re-expression and tamoxifen sensitivity, although sensitivity was not increased as robustly as expected. This could be due to increased cytoplasmic levels of HuR, suggesting that cytoplasmic HuR levels are central to tamoxifen responsiveness.
MeSH term(s)	Azacitidine/administration & dosage ; Azacitidine/analogs & derivatives ; Azacitidine/pharmacology ; Cell Line, Tumor ; Drug Administration Schedule ; Estrogen Receptor Modulators/administration & dosage ; Estrogen Receptor Modulators/pharmacology ; Humans ; Hydroxamic Acids/administration & dosage ; Hydroxamic Acids/pharmacology ; RNA, Messenger/genetics ; Receptors, Estrogen/genetics ; Tamoxifen/administration & dosage ; Tamoxifen/pharmacology
Chemical Substances	Estrogen Receptor Modulators ; Hydroxamic Acids ; RNA, Messenger ; Receptors, Estrogen ; Tamoxifen (094ZI81Y45) ; trichostatin A (3X2S926L3Z) ; decitabine (776B62CQ27) ; Azacitidine (M801H13NRU)
Language	English
Publishing date	2009-03-18
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2008.10.005
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Article: The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines

Licata, Lauren A / Hostetter, Christine L / Crismale, James / Sheth, Anjali / Keen, Judith Clancy

Breast cancer research and treatment. 2010 July, v. 122, no. 1

2010

Abstract: Meta-analyses of microarray data indicate that GATA3 is co-expressed with estrogen receptor alpha (ER) in breast cancer cells. While the significance of this remains unclear, it is thought that GATA3 may serve as a prognostic indicator in breast tumors ... ...

Abstract	Meta-analyses of microarray data indicate that GATA3 is co-expressed with estrogen receptor alpha (ER) in breast cancer cells. While the significance of this remains unclear, it is thought that GATA3 may serve as a prognostic indicator in breast tumors and may play a role in ER signaling. Recently, reciprocal regulation of GATA3 and ER transcription was demonstrated, suggesting that control of their expression is intertwined. We sought to determine whether GATA3 and ER expression was also coordinately regulated at other levels. Unlike ER, GATA3 was not under epigenetic control and was not re-expressed in the presence of DNMT or HDAC inhibitors in ER/GATA3-negative cells. However, like ER, these inhibitors decreased GATA3 expression in ER/GATA3-positive cell lines. We have previously reported that ER mRNA stability is increased through binding of the RNA-binding protein HuR/ELAV1 to the 3′untranslated region (UTR) and that DNMT and HDAC inhibitors reduce ER expression by altering this interaction. Biotin pull-down assays using a biotinylated GATA3 RNA probe confirmed that HuR also binds to the GATA3 3′UTR. Inhibition of HuR using siRNA probes decreased GATA3 mRNA, mRNA stability and protein expression, indicating that HuR plays a role in regulating GATA3 expression. Inhibition of either HuR or GATA3 reduced cell growth of MCF7 cells. Based on our findings, it is clear that coordinate regulation of ER and GATA3 occurs, however differences do exist. These findings may aid in identification of new targets that control cell growth of breast cancer cells.
Language	English
Dates of publication	2010-07
Size	p. 55-63.
Publisher	Springer US
Publishing place	Boston
Document type	Article
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-009-0517-8
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 1655: Show issues

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Article ; Online: The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines.

Licata, Lauren A / Hostetter, Christine L / Crismale, James / Sheth, Anjali / Keen, Judith Clancy

Breast cancer research and treatment

2009 Volume 122, Issue 1, Page(s) 55–63

Abstract	Meta-analyses of microarray data indicate that GATA3 is co-expressed with estrogen receptor alpha (ER) in breast cancer cells. While the significance of this remains unclear, it is thought that GATA3 may serve as a prognostic indicator in breast tumors and may play a role in ER signaling. Recently, reciprocal regulation of GATA3 and ER transcription was demonstrated, suggesting that control of their expression is intertwined. We sought to determine whether GATA3 and ER expression was also coordinately regulated at other levels. Unlike ER, GATA3 was not under epigenetic control and was not re-expressed in the presence of DNMT or HDAC inhibitors in ER/GATA3-negative cells. However, like ER, these inhibitors decreased GATA3 expression in ER/GATA3-positive cell lines. We have previously reported that ER mRNA stability is increased through binding of the RNA-binding protein HuR/ELAV1 to the 3'untranslated region (UTR) and that DNMT and HDAC inhibitors reduce ER expression by altering this interaction. Biotin pull-down assays using a biotinylated GATA3 RNA probe confirmed that HuR also binds to the GATA3 3'UTR. Inhibition of HuR using siRNA probes decreased GATA3 mRNA, mRNA stability and protein expression, indicating that HuR plays a role in regulating GATA3 expression. Inhibition of either HuR or GATA3 reduced cell growth of MCF7 cells. Based on our findings, it is clear that coordinate regulation of ER and GATA3 occurs, however differences do exist. These findings may aid in identification of new targets that control cell growth of breast cancer cells.
MeSH term(s)	3' Untranslated Regions ; Antigens, Surface/physiology ; Base Sequence ; Binding Sites ; Biotinylation ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor/drug effects ; Cell Line, Tumor/metabolism ; Consensus Sequence ; ELAV Proteins ; ELAV-Like Protein 1 ; Epigenesis, Genetic ; Estrogen Receptor alpha/biosynthesis ; Estrogen Receptor alpha/genetics ; Female ; GATA3 Transcription Factor/biosynthesis ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/physiology ; Gene Expression Regulation, Neoplastic ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Molecular Sequence Data ; Protein Binding ; RNA Stability/physiology ; RNA, Messenger/metabolism ; RNA, Neoplasm/metabolism ; RNA, Small Interfering/pharmacology ; RNA-Binding Proteins/physiology
Chemical Substances	3' Untranslated Regions ; Antigens, Surface ; ELAV Proteins ; ELAV-Like Protein 1 ; ELAVL1 protein, human ; ESR1 protein, human ; Estrogen Receptor alpha ; GATA3 Transcription Factor ; GATA3 protein, human ; Histone Deacetylase Inhibitors ; RNA, Messenger ; RNA, Neoplasm ; RNA, Small Interfering ; RNA-Binding Proteins
Language	English
Publishing date	2009-09-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-009-0517-8
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Article ; Online: Liver myeloid-derived suppressor cells expand in response to liver metastases in mice and inhibit the anti-tumor efficacy of anti-CEA CAR-T.

Burga, Rachel A / Thorn, Mitchell / Point, Gary R / Guha, Prajna / Nguyen, Cang T / Licata, Lauren A / DeMatteo, Ronald P / Ayala, Alfred / Joseph Espat, N / Junghans, Richard P / Katz, Steven C

Cancer immunology, immunotherapy : CII

2015 Volume 64, Issue 7, Page(s) 817–829

Abstract: Chimeric antigen receptor-modified T cell (CAR-T) technology, a promising immunotherapeutic tool, has not been applied specifically to treat liver metastases (LM). While CAR-T delivery to LM can be optimized by regional intrahepatic infusion, we propose ... ...

Abstract	Chimeric antigen receptor-modified T cell (CAR-T) technology, a promising immunotherapeutic tool, has not been applied specifically to treat liver metastases (LM). While CAR-T delivery to LM can be optimized by regional intrahepatic infusion, we propose that liver CD11b+Gr-1+ myeloid-derived suppressor cells (L-MDSC) will inhibit the efficacy of CAR-T in the intrahepatic space. We studied anti-CEA CAR-T in a murine model of CEA+ LM and identified mechanisms through which L-MDSC expand and inhibit CAR-T function. We established CEA+ LM in mice and studied purified L-MDSC and responses to treatment with intrahepatic anti-CEA CAR-T infusions. L-MDSC expanded threefold in response to LM, and their expansion was dependent on GM-CSF, which was produced by tumor cells. L-MDSC utilized PD-L1 to suppress anti-tumor responses through engagement of PD-1 on CAR-T. GM-CSF, in cooperation with STAT3, promoted L-MDSC PD-L1 expression. CAR-T efficacy was rescued when mice received CAR-T in combination with MDSC depletion, GM-CSF neutralization to prevent MDSC expansion, or PD-L1 blockade. As L-MDSC suppressed anti-CEA CAR-T, infusion of anti-CEA CAR-T in tandem with agents targeting L-MDSC is a rational strategy for future clinical trials.
MeSH term(s)	Animals ; B7-H1 Antigen/genetics ; B7-H1 Antigen/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Carcinoembryonic Antigen/immunology ; Cell Line, Tumor ; Disease Models, Animal ; Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis ; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Liver/cytology ; Liver/pathology ; Liver Neoplasms/pathology ; Liver Neoplasms/secondary ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid Cells/immunology ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/therapeutic use ; STAT3 Transcription Factor/metabolism ; Tumor Burden
Chemical Substances	B7-H1 Antigen ; Carcinoembryonic Antigen ; Cd274 protein, mouse ; Receptors, Antigen, T-Cell ; Recombinant Fusion Proteins ; STAT3 Transcription Factor ; Stat3 protein, mouse ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2015-07
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	195342-4
ISSN	1432-0851 ; 0340-7004
ISSN (online)	1432-0851
ISSN	0340-7004
DOI	10.1007/s00262-015-1692-6
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Zs.A 1237: Show issues

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Article ; Online: Biliary obstruction results in PD-1-dependent liver T cell dysfunction and acute inflammation mediated by Th17 cells and neutrophils.

Licata, Lauren A / Nguyen, Cang T / Burga, Rachel A / Falanga, Vincent / Espat, N Joseph / Ayala, Alfred / Thorn, Mitchell / Junghans, Richard P / Katz, Steven C

Journal of leukocyte biology

2013 Volume 94, Issue 4, Page(s) 813–823

Abstract: Biliary obstruction is a common clinical problem that is associated with intrahepatic inflammation and impaired immunity. PD-1 is well known to mediate T cell dysfunction but has been reported to promote and attenuate acute inflammation in various injury ...

Abstract	Biliary obstruction is a common clinical problem that is associated with intrahepatic inflammation and impaired immunity. PD-1 is well known to mediate T cell dysfunction but has been reported to promote and attenuate acute inflammation in various injury models. With the use of a well-established murine model of BDL, we studied the effects of intrahepatic PD-1 expression on LTC function, inflammation, and cholestasis. Following BDL, PD-1 expression increased significantly among LTCs. Increased PD-1 expression following BDL was associated with decreased LTC proliferation and less IFN-γ production. Elimination of PD-1 expression resulted in significantly improved proliferative capacity among LTC following BDL, in addition to a more immunostimulatory cytokine profile. Not only was LTC function rescued in PD-1(-/-) mice, but also, the degrees of biliary cell injury, cholestasis, and inflammation were diminished significantly compared with WT animals following BDL. PD-1-mediated acute inflammation following BDL was associated with expansions of intrahepatic neutrophil and Th17 cell populations, with the latter dependent on IL-6. PD-1 blockade represents an attractive strategy for reversing intrahepatic immunosuppression while limiting inflammatory liver damage.
MeSH term(s)	Animals ; Bile Ducts/metabolism ; Bile Ducts/pathology ; Cell Proliferation ; Cholestasis/complications ; Cholestasis/immunology ; Cholestasis/pathology ; Cholestasis/physiopathology ; Inflammation/complications ; Inflammation/immunology ; Inflammation/pathology ; Interleukin-6/metabolism ; Jaundice/complications ; Jaundice/immunology ; Jaundice/pathology ; Jaundice/physiopathology ; Ligation ; Liver/immunology ; Liver/pathology ; Liver/physiopathology ; Male ; Mice ; Mice, Inbred BALB C ; Neutrophils/immunology ; Neutrophils/pathology ; Programmed Cell Death 1 Receptor/metabolism ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Th17 Cells/pathology ; Up-Regulation
Chemical Substances	Interleukin-6 ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2013-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0313137
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Zs.A 603: Show issues

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Article ; Online: Anti-KIT designer T cells for the treatment of gastrointestinal stromal tumor.

Katz, Steven C / Burga, Rachel A / Naheed, Seema / Licata, Lauren A / Thorn, Mitchell / Osgood, Doreen / Nguyen, Cang T / Espat, N Joseph / Fletcher, Jonathan A / Junghans, Richard P

Journal of translational medicine

2013 Volume 11, Page(s) 46

Abstract: Background: Imatinib mesylate is an effective treatment for metastatic gastrointestinal stromal tumor (GIST). However, most patients eventually develop resistance and there are few other treatment options. Immunotherapy using genetically modified or ... ...

Abstract	Background: Imatinib mesylate is an effective treatment for metastatic gastrointestinal stromal tumor (GIST). However, most patients eventually develop resistance and there are few other treatment options. Immunotherapy using genetically modified or designer T cells (dTc) has gained increased attention for several malignancies in recent years. The aims of this study were to develop and test novel anti-KIT dTc engineered to target GIST cells. Methods: Human anti-KIT dTc were created by retroviral transduction with novel chimeric immune receptors (CIR). The gene for stem cell factor (SCF), the natural ligand for KIT, was cloned into 1st generation (SCF-CD3ζ, 1st gen) and 2nd generation (SCF-CD28-CD3ζ, 2nd gen) CIR constructs. In vitro dTc proliferation and tumoricidal capacity in the presence of KIT+ tumor cells were measured. In vivo assessment of dTc anti-tumor efficacy was performed by treating immunodeficient mice harboring subcutaneous GIST xenografts with dTc tail vein infusions. Results: We successfully produced the 1st and 2nd gen anti-KIT CIR and transduced murine and human T cells. Average transduction efficiencies for human 1st and 2nd gen dTc were 50% and 42%. When co-cultured with KIT+ tumor cells, both 1st and 2nd gen dTc proliferated and produced IFNγ. Human anti-KIT dTc were efficient at lysing GIST in vitro compared to untransduced T cells. In mice with established GIST xenografts, treatment with either 1st or 2nd gen human anti-KIT dTc led to significant reductions in tumor growth rates. Conclusions: We have constructed a novel anti-KIT CIR for production of dTc that possess specific activity against KIT+ GIST in vitro and in vivo. Further studies are warranted to evaluate the therapeutic potential and safety of anti-KIT dTc.
MeSH term(s)	Animals ; Base Sequence ; Cell Proliferation ; DNA Primers ; Gastrointestinal Stromal Tumors/pathology ; Gastrointestinal Stromal Tumors/therapy ; Male ; Mice ; Mice, Nude ; Polymerase Chain Reaction ; Proto-Oncogene Proteins c-kit/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology
Chemical Substances	DNA Primers ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2013-02-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1479-5876
ISSN (online)	1479-5876
DOI	10.1186/1479-5876-11-46
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Article ; Online: Cytoplasmic accumulation of the RNA binding protein HuR is central to tamoxifen resistance in estrogen receptor positive breast cancer cells.

Hostetter, Christine / Licata, Lauren A / Witkiewicz, Agnieszka / Costantino, Christina L / Yeo, Charles J / Brody, Jonathan R / Keen, Judith Clancy

Cancer biology & therapy

2008 Volume 7, Issue 9, Page(s) 1496–1506

Abstract: With prolonged exposure, a majority of estrogen receptor positive cancers develop resistance to tamoxifen and subsequent therapies including selective estrogen receptor modulators (SERMs) and aromatase inhibitors (AIs). While much is known about ... ...

Abstract	With prolonged exposure, a majority of estrogen receptor positive cancers develop resistance to tamoxifen and subsequent therapies including selective estrogen receptor modulators (SERMs) and aromatase inhibitors (AIs). While much is known about overexpression of key growth promoting receptors including EGF, erbB2/Her2 and IGF receptors and subsequent activation of MAPK signaling associated with resistance, the underlying mechanism in the development of resistance still remains unknown. We found that inhibition of JNK, a member of the MAPK family, decreases cytoplasmic accumulation of the RNA binding protein HuR. This data combined with previous reports that erbB2/Her2 and IGF-IR signals through JNK, led us to hypothesize that cytoplasmic accumulation of HuR may be a key contributor to development of tamoxifen resistance. Therefore, we tested the effect of HuR expression on tamoxifen responsiveness in both tamoxifen sensitive MCF7 and tamoxifen resistant BT474 cell lines. We found that decreasing the cytoplasmic HuR levels in the cells increases tamoxifen responsiveness in both cell lines. Conversely, the overexpression of HuR establishes tamoxifen resistance in MCF7 cells. Therefore, our data indicate that HuR is central to tamoxifen resistance. Interestingly, we found that acute exposure (24 and 48 h) of MCF7 cells to tamoxifen increased cytoplasmic levels of HuR and concomitantly it's ligand pp32, suggesting a novel molecular mechanism of resistance and acute response to tamoxifen through increased stability of mRNA transcripts that code for drug-resistant transcripts. Indeed, evaluation of primary breast tumors revealed a correlation between tumor grade, tamoxifen responsiveness and cytoplasmic HuR status. Therefore, inhibition of the cytoplasmic accumulation of HuR concomitantly with the administration of current therapeutics may be a successful treatment strategy. Our data describe a novel mechanism for the development of tamoxifen resistance and is the first study to identify an RNA binding protein as a key mediator of resistance in breast cancer cells.
MeSH term(s)	Antigens, Surface/genetics ; Antigens, Surface/metabolism ; Antineoplastic Agents, Hormonal/pharmacology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Cytoplasm/metabolism ; Drug Resistance, Neoplasm/drug effects ; ELAV Proteins ; ELAV-Like Protein 1 ; Female ; Humans ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Receptors, Estrogen/drug effects ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Tamoxifen/pharmacology
Chemical Substances	Antigens, Surface ; Antineoplastic Agents, Hormonal ; ELAV Proteins ; ELAV-Like Protein 1 ; ELAVL1 protein, human ; RNA-Binding Proteins ; Receptors, Estrogen ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2008-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.4161/cbt.7.9.6490
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Article ; Online: Timing is everything: order of administration of 5-aza 2' deoxycytidine, trichostatin A and tamoxifen changes estrogen receptor mRNA expression and cell sensitivity.

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Article: The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines

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Article ; Online: The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines.

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Article ; Online: Liver myeloid-derived suppressor cells expand in response to liver metastases in mice and inhibit the anti-tumor efficacy of anti-CEA CAR-T.

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Article ; Online: Biliary obstruction results in PD-1-dependent liver T cell dysfunction and acute inflammation mediated by Th17 cells and neutrophils.

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Article ; Online: Anti-KIT designer T cells for the treatment of gastrointestinal stromal tumor.

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Article ; Online: Cytoplasmic accumulation of the RNA binding protein HuR is central to tamoxifen resistance in estrogen receptor positive breast cancer cells.

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