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Article ; Online: Immunosuppressive Myeloid Cells Induce Nitric Oxide-Dependent DNA Damage and p53 Pathway Activation in CD8

Cartwright, Adam N R / Suo, Shengbao / Badrinath, Soumya / Kumar, Sushil / Melms, Johannes / Luoma, Adrienne / Bagati, Archis / Saadatpour, Assieh / Izar, Benjamin / Yuan, Guo-Cheng / Wucherpfennig, Kai W

Cancer immunology research

2021 Volume 9, Issue 4, Page(s) 470–485

Abstract: Tumor-infiltrating myeloid-derived suppressor cells (MDSC) are associated with poor survival outcomes in many human cancers. MDSCs inhibit T cell-mediated tumor immunity in part because they strongly inhibit T-cell function. However, whether MDSCs ... ...

Abstract	Tumor-infiltrating myeloid-derived suppressor cells (MDSC) are associated with poor survival outcomes in many human cancers. MDSCs inhibit T cell-mediated tumor immunity in part because they strongly inhibit T-cell function. However, whether MDSCs inhibit early or later steps of T-cell activation is not well established. Here we show that MDSCs inhibited proliferation and induced apoptosis of CD8
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; DNA Damage ; Humans ; Immunosuppressive Agents ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Myeloid-Derived Suppressor Cells/immunology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Signal Transduction/immunology ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Immunosuppressive Agents ; Tumor Suppressor Protein p53 ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2021-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-20-0085
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Article ; Online: Potassium channels in Drosophila: historical breakthroughs, significance, and perspectives.

Frolov, Roman V / Bagati, Archis / Casino, Brittany / Singh, Satpal

Journal of neurogenetics

2012 Volume 26, Issue 3-4, Page(s) 275–290

Abstract: Drosophila has enabled important breakthroughs in K(+) channel research, including identification and fi rst cloning of a voltage-activated K(+) channel, Shaker, a founding member of the K(V)1 family. Drosophila has also helped in discovering other K(+) ... ...

Abstract	Drosophila has enabled important breakthroughs in K(+) channel research, including identification and fi rst cloning of a voltage-activated K(+) channel, Shaker, a founding member of the K(V)1 family. Drosophila has also helped in discovering other K(+) channels, such as Shab, Shaw, Shal, Eag, Sei, Elk, and also Slo, a Ca(2+) - and voltage-dependent K(+) channel. These findings have contributed significantly to our understanding of ion channels and their role in physiology. Drosophila continues to play an important role in ion channel studies, benefiting from an unparalleled arsenal of genetic tools and availability of tens of thousands of genetically modified strains. These tools allow deletion, expression, or misexpression of almost any gene in question with temporal and spatial control. The combination of these tools and resources with the use of forward genetic approach in Drosophila further enhances its strength as a model system. There are many areas in which Drosophila can further help our understanding of ion channels and their function. These include signaling pathways involved in regulating and modulating ion channels, basic information on channels and currents where very little is currently known, and the role of ion channels in physiology and pathology.
MeSH term(s)	Animals ; Channelopathies/genetics ; Channelopathies/history ; Drosophila ; Drosophila Proteins/history ; Drosophila Proteins/physiology ; History, 20th Century ; Mutation/genetics ; Potassium Channels/history ; Potassium Channels/physiology ; Signal Transduction/physiology
Chemical Substances	Drosophila Proteins ; Potassium Channels
Language	English
Publishing date	2012-09
Publishing country	England
Document type	Historical Article ; Journal Article ; Review
ZDB-ID	605543-6
ISSN	1563-5260 ; 0167-7063
ISSN (online)	1563-5260
ISSN	0167-7063
DOI	10.3109/01677063.2012.744990
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Zs.A 1878: Show issues

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Article: A modified In vitro invasion assay to determine the potential role of hormones, cytokines and/or growth factors in mediating cancer cell invasion

Bagati, Archis / Koch, Zethan / Bofinger, Diane / Goli, Haneesha / Weiss, Laura S / Dau, Rosie / Thomas, Megha / Zucker, Shoshanna N

Journal of visualized experiments. 2015 Apr. 24, , no. 98

2015

Abstract: Blood serum serves as a chemoattractant towards which cancer cells migrate and invade, facilitating their intravasation into microvessels. However, the actual molecules towards which the cells migrate remain elusive. This modified invasion assay has been ...

Abstract	Blood serum serves as a chemoattractant towards which cancer cells migrate and invade, facilitating their intravasation into microvessels. However, the actual molecules towards which the cells migrate remain elusive. This modified invasion assay has been developed to identify targets which drive cell migration and invasion. This technique compares the invasion index under three conditions to determine whether a specific hormone, growth factor, or cytokine plays a role in mediating the invasive potential of a cancer cell. These conditions include i) normal fetal bovine serum (FBS), ii) charcoal-stripped FBS (CS-FBS), which removes hormones, growth factors, and cytokines and iii) CS-FBS + molecule (denoted “X”). A significant change in cell invasion with CS-FBS as compared to FBS, indicates the involvement of hormones, cytokines or growth factors in mediating the change. Individual molecules can then be added back to CS-FBS to assay their ability to reverse or rescue the invasion phenotype. Furthermore, two or more factors can be combined to evaluate the additive or synergistic effects of multiple molecules in driving or inhibiting invasion. Overall, this method enables the investigator to determine whether hormones, cytokines, and/or growth factors play a role in cell invasion by serving as chemoattractants or inhibitors of invasion for a particular type of cancer cell or a specific mutant. By identifying specific chemoattractants and inhibitors, this modified invasion assay may help to elucidate signaling pathways that direct cancer cell invasion.
Keywords	cell movement ; chemoattractants ; cytokines ; fetal bovine serum ; growth factors ; hormones ; mutants ; neoplasm cells ; neoplasms ; phenotype ; signal transduction ; synergism
Language	English
Dates of publication	2015-0424
Size	p. e51480.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/51480
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Novel combination therapy for melanoma induces apoptosis via a gap junction positive feedback mechanism.

Bagati, Archis / Hutcherson, Timothy C / Koch, Zethan / Pechette, Joseph / Dianat, Hossein / Higley, Cory / Chiu, Lisa / Song, Yesul / Shah, Jay / Chazen, Elana / Nicolais, Andrew / Casey, Peter / Thompson, Kyle / Burke, Kevin / Nikiforov, Mikhail A / Zirnheld, Jennifer / Zucker, Shoshanna N

Oncotarget

2020 Volume 11, Issue 37, Page(s) 3443–3458

Abstract: Metastatic melanoma cells overexpressing gap junctions were assayed for their ability to propagate cell death by a novel combination therapy that generates reactive oxygen species (ROS) by both 1) non-thermal plasma (NTP) and 2) tirapazamine (TPZ) under ... ...

Abstract	Metastatic melanoma cells overexpressing gap junctions were assayed for their ability to propagate cell death by a novel combination therapy that generates reactive oxygen species (ROS) by both 1) non-thermal plasma (NTP) and 2) tirapazamine (TPZ) under hypoxic conditions. Results demonstrate additive-to-synergistic effects of combination therapy compared to each agent individually. NTP induces highly localized cell death in target areas whereas TPZ partially reduces viability over the total surface area. However, when high gap junction expression was induced in melanoma cells, effects of combination NTP+TPZ therapy was augmented, spreading cell death across the entire plate. Similarly,
Language	English
Publishing date	2020-09-15
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.27732
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Article ; Online: Integrin αvβ6-TGFβ-SOX4 Pathway Drives Immune Evasion in Triple-Negative Breast Cancer.

Bagati, Archis / Kumar, Sushil / Jiang, Peng / Pyrdol, Jason / Zou, Angela E / Godicelj, Anze / Mathewson, Nathan D / Cartwright, Adam N R / Cejas, Paloma / Brown, Myles / Giobbie-Hurder, Anita / Dillon, Deborah / Agudo, Judith / Mittendorf, Elizabeth A / Liu, X Shirley / Wucherpfennig, Kai W

Cancer cell

2020 Volume 39, Issue 1, Page(s) 54–67.e9

Abstract: Cancer immunotherapy shows limited efficacy against many solid tumors that originate from epithelial tissues, including triple-negative breast cancer (TNBC). We identify the SOX4 transcription factor as an important resistance mechanism to T cell- ... ...

Abstract	Cancer immunotherapy shows limited efficacy against many solid tumors that originate from epithelial tissues, including triple-negative breast cancer (TNBC). We identify the SOX4 transcription factor as an important resistance mechanism to T cell-mediated cytotoxicity for TNBC cells. Mechanistic studies demonstrate that inactivation of SOX4 in tumor cells increases the expression of genes in a number of innate and adaptive immune pathways important for protective tumor immunity. Expression of SOX4 is regulated by the integrin αvβ6 receptor on the surface of tumor cells, which activates TGFβ from a latent precursor. An integrin αvβ6/8-blocking monoclonal antibody (mAb) inhibits SOX4 expression and sensitizes TNBC cells to cytotoxic T cells. This integrin mAb induces a substantial survival benefit in highly metastatic murine TNBC models poorly responsive to PD-1 blockade. Targeting of the integrin αvβ6-TGFβ-SOX4 pathway therefore provides therapeutic opportunities for TNBC and other highly aggressive human cancers of epithelial origin.
MeSH term(s)	Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/pharmacology ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/metabolism ; Antineoplastic Agents, Immunological/therapeutic use ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Integrins/antagonists & inhibitors ; Integrins/genetics ; Integrins/metabolism ; Mice ; Neoplasm Transplantation ; SOXC Transcription Factors/genetics ; SOXC Transcription Factors/metabolism ; Sequence Analysis, RNA ; Signal Transduction/drug effects ; T-Lymphocytes, Cytotoxic/drug effects ; T-Lymphocytes, Cytotoxic/metabolism ; Transforming Growth Factor beta/genetics ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/immunology ; Tumor Escape/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Monoclonal ; Antigens, Neoplasm ; Antineoplastic Agents, Immunological ; Integrins ; SOX4 protein, human ; SOXC Transcription Factors ; Transforming Growth Factor beta ; integrin alphavbeta6
Language	English
Publishing date	2020-12-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2020.12.001
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article ; Online: CARM1 Inhibition Enables Immunotherapy of Resistant Tumors by Dual Action on Tumor Cells and T Cells.

Cancer discovery

2021 Volume 11, Issue 8, Page(s) 2050–2071

Abstract: A number of cancer drugs activate innate immune pathways in tumor cells but unfortunately also compromise antitumor immune function. We discovered that inhibition of CARM1, an epigenetic enzyme and cotranscriptional activator, elicited beneficial ... ...

Abstract	A number of cancer drugs activate innate immune pathways in tumor cells but unfortunately also compromise antitumor immune function. We discovered that inhibition of CARM1, an epigenetic enzyme and cotranscriptional activator, elicited beneficial antitumor activity in both cytotoxic T cells and tumor cells. In T cells,
MeSH term(s)	Cell Line, Tumor/drug effects ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immunotherapy ; Neoplasms/therapy ; Protein-Arginine N-Methyltransferases/antagonists & inhibitors ; T-Lymphocytes/drug effects
Chemical Substances	Immune Checkpoint Inhibitors ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319) ; coactivator-associated arginine methyltransferase 1 (EC 2.1.1.319)
Language	English
Publishing date	2021-03-11
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	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-1144
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Zs.A 6916: Show issues

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Article ; Online: XBP1-KLF9 Axis Acts as a Molecular Rheostat to Control the Transition from Adaptive to Cytotoxic Unfolded Protein Response.

Fink, Emily E / Moparthy, Sudha / Bagati, Archis / Bianchi-Smiraglia, Anna / Lipchick, Brittany C / Wolff, David W / Roll, Matthew V / Wang, Jianmin / Liu, Song / Bakin, Andrei V / Kandel, Eugene S / Lee, Ann-Hwee / Nikiforov, Mikhail A

Cell reports

2018 Volume 25, Issue 1, Page(s) 212–223.e4

Abstract: Transcription factor XBP1s, activated by endoplasmic reticulum (ER) stress in a dose-dependent manner, plays a central role in adaptive unfolded protein response (UPR) via direct activation of multiple genes controlling protein refolding. Here, we report ...

Abstract	Transcription factor XBP1s, activated by endoplasmic reticulum (ER) stress in a dose-dependent manner, plays a central role in adaptive unfolded protein response (UPR) via direct activation of multiple genes controlling protein refolding. Here, we report that elevation of ER stress above a critical threshold causes accumulation of XBP1s protein sufficient for binding to the promoter and activation of a gene encoding a transcription factor KLF9. In comparison to other XBP1s targets, KLF9 promoter contains an evolutionary conserved lower-affinity binding site that requires higher amounts of XBP1s for activation. In turn, KLF9 induces expression of two regulators of ER calcium storage, TMEM38B and ITPR1, facilitating additional calcium release from ER, exacerbation of ER stress, and cell death. Accordingly, Klf9 deficiency attenuates tunicamycin-induced ER stress in mouse liver. These data reveal a role for XBP1s in cytotoxic UPR and provide insights into mechanisms of life-or-death decisions in cells under ER stress.
MeSH term(s)	Animals ; Endoplasmic Reticulum Stress ; Female ; HCT116 Cells ; HEK293 Cells ; Humans ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Unfolded Protein Response/physiology ; Up-Regulation ; X-Box Binding Protein 1/genetics ; X-Box Binding Protein 1/metabolism
Chemical Substances	KLF9 protein, human ; Klf9 protein, mouse ; Kruppel-Like Transcription Factors ; RNA, Messenger ; X-Box Binding Protein 1 ; XBP1 protein, human ; Xbp1 protein, mouse
Language	English
Publishing date	2018-09-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.09.013
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Article ; Online: A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion.

Bagati, Archis / Koch, Zethan / Bofinger, Diane / Goli, Haneesha / Weiss, Laura S / Dau, Rosie / Thomas, Megha / Zucker, Shoshanna N

Journal of visualized experiments : JoVE

2015 , Issue 98

Abstract	Blood serum serves as a chemoattractant towards which cancer cells migrate and invade, facilitating their intravasation into microvessels. However, the actual molecules towards which the cells migrate remain elusive. This modified invasion assay has been developed to identify targets which drive cell migration and invasion. This technique compares the invasion index under three conditions to determine whether a specific hormone, growth factor, or cytokine plays a role in mediating the invasive potential of a cancer cell. These conditions include i) normal fetal bovine serum (FBS), ii) charcoal-stripped FBS (CS-FBS), which removes hormones, growth factors, and cytokines and iii) CS-FBS + molecule (denoted "X"). A significant change in cell invasion with CS-FBS as compared to FBS, indicates the involvement of hormones, cytokines or growth factors in mediating the change. Individual molecules can then be added back to CS-FBS to assay their ability to reverse or rescue the invasion phenotype. Furthermore, two or more factors can be combined to evaluate the additive or synergistic effects of multiple molecules in driving or inhibiting invasion. Overall, this method enables the investigator to determine whether hormones, cytokines, and/or growth factors play a role in cell invasion by serving as chemoattractants or inhibitors of invasion for a particular type of cancer cell or a specific mutant. By identifying specific chemoattractants and inhibitors, this modified invasion assay may help to elucidate signaling pathways that direct cancer cell invasion.
MeSH term(s)	Animals ; Cattle ; Cell Culture Techniques/methods ; Cell Line, Tumor ; Cell Movement/physiology ; Culture Media ; Cytokines/pharmacology ; Cytokines/physiology ; Hormones/pharmacology ; Hormones/physiology ; Humans ; In Vitro Techniques ; Intercellular Signaling Peptides and Proteins/pharmacology ; Neoplasm Invasiveness ; Neoplasms/pathology
Chemical Substances	Culture Media ; Cytokines ; Hormones ; Intercellular Signaling Peptides and Proteins
Language	English
Publishing date	2015-04-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/51480
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Article ; Online: A dominant negative Cx43 mutant differentially affects tumorigenic and invasive properties in human metastatic melanoma cells.

Zucker, Shoshanna N / Bancroft, Tara A / Place, David E / Des Soye, Benjamin / Bagati, Archis / Berezney, Ronald

Journal of cellular physiology

2013 Volume 228, Issue 4, Page(s) 853–859

Abstract: Previous reports have implicated connexin 43 (Cx43) as a tumor suppressor in early stages of tumorigenesis and in some cases as an enhancer of cell migration in later stages. To address the role of Cx43 in melanoma tumor progression, we utilized two ... ...

Abstract	Previous reports have implicated connexin 43 (Cx43) as a tumor suppressor in early stages of tumorigenesis and in some cases as an enhancer of cell migration in later stages. To address the role of Cx43 in melanoma tumor progression, we utilized two melanoma cell lines derived from the same patient in pre-metastasis (WM793B) and following isolation from a lung metastasis in nude mice (1205Lu). Our results demonstrate a strikingly increased expression of Cx43 in both the pre-metastatic and metastatic melanoma cell lines that were actively migrating compared to non-migrating cells. To further investigate the role of Cx43 in these melanoma cells, we overexpressed wild type (wt) Cx43 as well as a mutant dominant negative Cx43 mutant that causes closed channels (T154A). The metastatic 1205Lu cells expressing Cx43-T154A showed a twofold decrease in colony formation on soft agar while the nonmetastatic WM793B cells showed no significant change. In invasion assays through a collagen matrix, the same Cx43-T154A 1205Lu cells demonstrated a three- to fourfold increase in the invasion index compared to either wt Cx43 or vector control cells. The increase in invasiveness was eliminated by migration towards media with charcoal-stripped serum, suggesting that migration may be directed towards a lipophilic compound(s). Our findings demonstrate that a dominant negative Cx43 mutant deficient in channel formation exhibits a dual pattern of regulation in metastatic melanoma cells with a decrease in anchorage-independent growth and an increase in invasive potential.
MeSH term(s)	Animals ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Connexin 43/genetics ; Connexin 43/metabolism ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; Mice, Nude ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology
Chemical Substances	Connexin 43
Language	English
Publishing date	2013-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.24235
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Article ; Online: KLF9-dependent ROS regulate melanoma progression in stage-specific manner.

Oncogene

2019 Volume 38, Issue 19, Page(s) 3585–3597

Abstract: Although antioxidants promote melanoma metastasis, the role of reactive oxygen species (ROS) in other stages of melanoma progression is controversial. Moreover, genes regulating ROS have not been functionally characterized throughout the entire tumor ... ...

Abstract	Although antioxidants promote melanoma metastasis, the role of reactive oxygen species (ROS) in other stages of melanoma progression is controversial. Moreover, genes regulating ROS have not been functionally characterized throughout the entire tumor progression in mouse models of cancer. To address this question, we crossed mice-bearing knock-out of Klf9, an ubiquitous transcriptional regulator of oxidative stress, with two conditional melanocytic mouse models: Braf
MeSH term(s)	Acetylcysteine/adverse effects ; Adult ; Aged ; Aged, 80 and over ; Animals ; Humans ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Melanocytes/drug effects ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Melanoma, Experimental/chemically induced ; Melanoma, Experimental/metabolism ; Melanoma, Experimental/pathology ; Mice, Knockout ; Middle Aged ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Reactive Oxygen Species/metabolism ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology
Chemical Substances	KLF9 protein, human ; Klf9 protein, mouse ; Kruppel-Like Transcription Factors ; Reactive Oxygen Species ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2019-01-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-019-0689-6
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