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Article ; Online: Fatty acid oxidation protects cancer cells from apoptosis by increasing mitochondrial membrane lipids.

Li, Yi-Jia / Fahrmann, Johannes Francois / Aftabizadeh, Maryam / Zhao, Qianqian / Tripathi, Satyendra C / Zhang, Chunyan / Yuan, Yuan / Ann, David / Hanash, Samir / Yu, Hua

Cell reports

2022 Volume 39, Issue 13, Page(s) 111044

Language	English
Publishing date	2022-07-06
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111044
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Article ; Online: Fatty acid oxidation protects cancer cells from apoptosis by increasing mitochondrial membrane lipids.

Li, Yi-Jia / Fahrmann, Johannes Francois / Aftabizadeh, Maryam / Zhao, Qianqian / Tripathi, Satyendra C / Zhang, Chunyan / Yuan, Yuan / Ann, David / Hanash, Samir / Yu, Hua

Cell reports

2022 Volume 39, Issue 9, Page(s) 110870

Abstract: Overcoming resistance to chemotherapies remains a major unmet need for cancers, such as triple-negative breast cancer (TNBC). Therefore, mechanistic studies to provide insight for drug development are urgently needed to overcome TNBC therapy resistance. ... ...

Abstract	Overcoming resistance to chemotherapies remains a major unmet need for cancers, such as triple-negative breast cancer (TNBC). Therefore, mechanistic studies to provide insight for drug development are urgently needed to overcome TNBC therapy resistance. Recently, an important role of fatty acid β-oxidation (FAO) in chemoresistance has been shown. But how FAO might mitigate tumor cell apoptosis by chemotherapy is unclear. Here, we show that elevated FAO activates STAT3 by acetylation via elevated acetyl-coenzyme A (CoA). Acetylated STAT3 upregulates expression of long-chain acyl-CoA synthetase 4 (ACSL4), resulting in increased phospholipid synthesis. Elevating phospholipids in mitochondrial membranes leads to heightened mitochondrial integrity, which in turn overcomes chemotherapy-induced tumor cell apoptosis. Conversely, in both cultured tumor cells and xenograft tumors, enhanced cancer cell apoptosis by inhibiting ASCL4 or specifically targeting acetylated-STAT3 is associated with a reduction in phospholipids within mitochondrial membranes. This study demonstrates a critical mechanism underlying tumor cell chemoresistance.
MeSH term(s)	Acetyl Coenzyme A/metabolism ; Apoptosis ; Fatty Acids/metabolism ; Humans ; Membrane Lipids/metabolism ; Mitochondrial Membranes/metabolism ; Oxidation-Reduction ; Phospholipids/metabolism ; Triple Negative Breast Neoplasms/metabolism
Chemical Substances	Fatty Acids ; Membrane Lipids ; Phospholipids ; Acetyl Coenzyme A (72-89-9)
Language	English
Publishing date	2022-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110870
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Article ; Online: Blocking Inflammasome Activation Caused by β-Amyloid Peptide (Aβ) and Islet Amyloid Polypeptide (IAPP) through an IAPP Mimic.

Aftabizadeh, Maryam / Tatarek-Nossol, Marianna / Andreetto, Erika / El Bounkari, Omar / Kipp, Markus / Beyer, Cordian / Latz, Eicke / Bernhagen, Jürgen / Kapurniotu, Aphrodite

ACS chemical neuroscience

2019 Volume 10, Issue 8, Page(s) 3703–3717

Abstract: Inflammation in the brain and pancreas is linked to cell degeneration and pathogenesis of both Alzheimer's disease (AD) and type 2 diabetes (T2D). Inflammatory cascades in both tissues are triggered by the uptake of β-amyloid peptide (Aβ) or islet ... ...

Abstract	Inflammation in the brain and pancreas is linked to cell degeneration and pathogenesis of both Alzheimer's disease (AD) and type 2 diabetes (T2D). Inflammatory cascades in both tissues are triggered by the uptake of β-amyloid peptide (Aβ) or islet amyloid polypeptide (IAPP) aggregates by microglial cells (AD) or macrophages (T2D) and their insufficient lysosomal degradation. This results in lysosomal damage, caspase-1/NLRP3 inflammasome activation and release of interleukin-1β (IL-1β), a key proinflammatory cytokine in both diseases. Here we show that the inflammatory processes mediated by Aβ and IAPP aggregates in microglial cells and macrophages are blocked by IAPP-GI, a nonamyloidogenic IAPP mimic, which forms high-affinity soluble and nonfibrillar hetero-oligomers with both polypeptides. In contrast to fibrillar Aβ aggregates, nonfibrillar Aβ/IAPP-GI or Aβ/IAPP hetero-oligomers become rapidly internalized by microglial cells and targeted to lysosomes where Aβ is fully degraded. Internalization occurs via IAPP receptor-mediated endocytosis. Moreover, in contrast to IAPP aggregates, IAPP/IAPP-GI hetero-oligomers become rapidly internalized and degraded in the lysosomal compartments of macrophages. Our findings uncover a previously unknown function for the IAPP/Aβ cross-amyloid interaction and suggest that conversion of Aβ or IAPP into lysosome-targeted and easily degradable hetero-oligomers by heteroassociation with IAPP mimics could become a promising approach to specifically prevent amyloid-mediated inflammation in AD, T2D, or both diseases.
MeSH term(s)	Amyloid/pharmacology ; Amyloid beta-Peptides/metabolism ; Animals ; Caspase 1/metabolism ; Cell Line ; Inflammasomes/metabolism ; Inflammation/metabolism ; Interleukin-1beta/metabolism ; Islet Amyloid Polypeptide/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Mice ; Microglia/drug effects ; Microglia/metabolism ; Peptidomimetics/pharmacology
Chemical Substances	(N-Me)G24, (N-Me)I26-IAPP ; Amyloid ; Amyloid beta-Peptides ; Inflammasomes ; Interleukin-1beta ; Islet Amyloid Polypeptide ; Peptidomimetics ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2019-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1948-7193
ISSN (online)	1948-7193
DOI	10.1021/acschemneuro.9b00260
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Article ; Online: Author Correction: Locoregional delivery of IL-13Rα2-targeting CAR-T cells in recurrent high-grade glioma: a phase 1 trial.

Brown, Christine E / Hibbard, Jonathan C / Alizadeh, Darya / Blanchard, M Suzette / Natri, Heini M / Wang, Dongrui / Ostberg, Julie R / Aguilar, Brenda / Wagner, Jamie R / Paul, Jinny A / Starr, Renate / Wong, Robyn A / Chen, Wuyang / Shulkin, Noah / Aftabizadeh, Maryam / Filippov, Aleksandr / Chaudhry, Ammar / Ressler, Julie A / Kilpatrick, Julie /

Myers-McNamara, Paige / Chen, Mike / Wang, Leo D / Rockne, Russell C / Georges, Joseph / Portnow, Jana / Barish, Michael E / D'Apuzzo, Massimo / Banovich, Nicholas E / Forman, Stephen J / Badie, Behnam

Nature medicine

2024

Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-024-02928-5
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Article ; Online: Locoregional delivery of IL-13Rα2-targeting CAR-T cells in recurrent high-grade glioma: a phase 1 trial.

Nature medicine

2024 Volume 30, Issue 4, Page(s) 1001–1012

Abstract: Chimeric antigen receptor T cell (CAR-T) therapy is an emerging strategy to improve treatment outcomes for recurrent high-grade glioma, a cancer that responds poorly to current therapies. Here we report a completed phase I trial evaluating IL-13Rα2- ... ...

Abstract	Chimeric antigen receptor T cell (CAR-T) therapy is an emerging strategy to improve treatment outcomes for recurrent high-grade glioma, a cancer that responds poorly to current therapies. Here we report a completed phase I trial evaluating IL-13Rα2-targeted CAR-T cells in 65 patients with recurrent high-grade glioma, the majority being recurrent glioblastoma (rGBM). Primary objectives were safety and feasibility, maximum tolerated dose/maximum feasible dose and a recommended phase 2 dose plan. Secondary objectives included overall survival, disease response, cytokine dynamics and tumor immune contexture biomarkers. This trial evolved to evaluate three routes of locoregional T cell administration (intratumoral (ICT), intraventricular (ICV) and dual ICT/ICV) and two manufacturing platforms, culminating in arm 5, which utilized dual ICT/ICV delivery and an optimized manufacturing process. Locoregional CAR-T cell administration was feasible and well tolerated, and as there were no dose-limiting toxicities across all arms, a maximum tolerated dose was not determined. Probable treatment-related grade 3+ toxicities were one grade 3 encephalopathy and one grade 3 ataxia. A clinical maximum feasible dose of 200 × 10
MeSH term(s)	Humans ; Receptors, Chimeric Antigen ; Neoplasm Recurrence, Local ; Glioma/therapy ; T-Lymphocytes ; Glioblastoma/therapy ; Immunotherapy, Adoptive/adverse effects ; Immunotherapy, Adoptive/methods
Chemical Substances	Receptors, Chimeric Antigen
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-024-02875-1
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Zs.A 4212: 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)
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Article ; Online: Potent antitumor effects of cell-penetrating peptides targeting STAT3 axis.

Aftabizadeh, Maryam / Li, Yi-Jia / Zhao, Qianqian / Zhang, Chunyan / Ambaye, Nigus / Song, Jieun / Nagao, Toshikage / Lahtz, Christoph / Fakih, Marwan / Ann, David K / Yu, Hua / Herrmann, Andreas

JCI insight

2021 Volume 6, Issue 2

Abstract: To date, there are no inhibitors that directly and specifically target activated STAT3 and c-Myc in the clinic. Although peptide-based inhibitors can selectively block activated targets, their clinical usage is limited because of low cell penetration and/ ...

Abstract	To date, there are no inhibitors that directly and specifically target activated STAT3 and c-Myc in the clinic. Although peptide-based inhibitors can selectively block activated targets, their clinical usage is limited because of low cell penetration and/or serum stability. Here, we generated cell-penetrating acetylated (acet.) STAT3, c-Myc, and Gp130 targeting peptides by attaching phosphorothioated (PS) polymer backbone to peptides. The cell-penetrating peptides efficiently penetrated cells and inhibited activation of the intended targets and their downstream genes. Locally or systemically treating tumor-bearing mice with PS-acet.-STAT3 peptide at low concentrations effectively blocked STAT3 in vivo, resulting in significant antitumor effects in 2 human xenograft models. Moreover, PS-acet.-STAT3 peptide penetrated and activated splenic CD8+ T cells in vitro. Treating immune-competent mice bearing mouse melanoma with PS-acet.-STAT3 peptide inhibited STAT3 in tumor-infiltrating T cells, downregulating tumor-infiltrating CD4+ T regulatory cells while activating CD8+ T effector cells. Similarly, systemic injections of the cell-penetrating c-Myc and Gp130 peptides prevented pancreatic tumor growth and induced antitumor immune responses. Taken together, we have developed therapeutic peptides that effectively and specifically block challenging cancer targets, resulting in antitumor effects through both direct tumor cell killing and indirectly through antitumor immune responses.
MeSH term(s)	Acetylation ; Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell-Penetrating Peptides/chemistry ; Cell-Penetrating Peptides/pharmacology ; Cytokine Receptor gp130/chemistry ; Drug Design ; HCT116 Cells ; Humans ; Lymphocytes, Tumor-Infiltrating/drug effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/immunology ; Melanoma, Experimental/metabolism ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/drug therapy ; Peptide Fragments/chemistry ; Peptide Fragments/pharmacology ; Protein Multimerization ; Proto-Oncogene Proteins c-myc/chemistry ; Proto-Oncogene Proteins c-myc/pharmacology ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/chemistry ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Cell-Penetrating Peptides ; MYC protein, human ; Peptide Fragments ; Proto-Oncogene Proteins c-myc ; STAT3 Transcription Factor ; STAT3 protein, human ; Stat3 protein, mouse ; Cytokine Receptor gp130 (133483-10-0)
Language	English
Publishing date	2021-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.136176
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Article ; Online: IFNγ Is Critical for CAR T Cell-Mediated Myeloid Activation and Induction of Endogenous Immunity.

Alizadeh, Darya / Wong, Robyn A / Gholamin, Sharareh / Maker, Madeleine / Aftabizadeh, Maryam / Yang, Xin / Pecoraro, Joseph R / Jeppson, John D / Wang, Dongrui / Aguilar, Brenda / Starr, Renate / Larmonier, Claire B / Larmonier, Nicolas / Chen, Min-Hsuan / Wu, Xiwei / Ribas, Antoni / Badie, Behnam / Forman, Stephen J / Brown, Christine E

Cancer discovery

2021 Volume 11, Issue 9, Page(s) 2248–2265

Abstract: Chimeric antigen receptor (CAR) T cells mediate potent antigen-specific antitumor activity; however, their indirect effects on the endogenous immune system are not well characterized. Remarkably, we demonstrate that CAR T-cell treatment of mouse ... ...

Abstract	Chimeric antigen receptor (CAR) T cells mediate potent antigen-specific antitumor activity; however, their indirect effects on the endogenous immune system are not well characterized. Remarkably, we demonstrate that CAR T-cell treatment of mouse syngeneic glioblastoma (GBM) activates intratumoral myeloid cells and induces endogenous T-cell memory responses coupled with feed-forward propagation of CAR T-cell responses. IFNγ production by CAR T cells and IFNγ responsiveness of host immune cells are critical for tumor immune landscape remodeling to promote a more activated and less suppressive tumor microenvironment. The clinical relevance of these observations is supported by studies showing that human IL13Rα2-CAR T cells activate patient-derived endogenous T cells and monocytes/macrophages through IFNγ signaling and induce the generation of tumor-specific T-cell responses in a responding patient with GBM. These studies establish that CAR T-cell therapy has the potential to shape the tumor microenvironment, creating a context permissible for eliciting endogenous antitumor immunity. SIGNIFICANCE: Our findings highlight the critical role of IFNγ signaling for a productive CAR T-cell therapy in GBM. We establish that CAR T cells can activate resident myeloid populations and promote endogenous T-cell immunity, emphasizing the importance of host innate and adaptive immunity for CAR T-cell therapy of solid tumors.
MeSH term(s)	Animals ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Immunotherapy, Adoptive ; Interferon-gamma/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Myeloid Cells/immunology ; Receptors, Chimeric Antigen/immunology ; Tumor Microenvironment ; Xenograft Model Antitumor Assays
Chemical Substances	Receptors, Chimeric Antigen ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2021-04-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-1661
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Zs.A 6916: Show issues

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Article: Expansion of endogenous T cells in CSF of pediatric CNS tumor patients undergoing locoregional delivery of IL13R〿2-targeting CAR T cells: an interim analysis.

Wang, Leo / Oill, Angela Taravella / Blanchard, M / Wu, Melody / Hibbard, Jonathan / Sepulveda, Sean / Peter, Lance / Kilpatrick, Julie / Munoz, Margarita / Stiller, Tracey / Shulkin, Noah / Wagner, Jamie / Dolatabadi, Ally / Nisis, Monica / Shepphird, Jennifer / Sanchez, Gabriela / Lingaraju, Chetan / Manchanda, Mishika / Natri, Heini /

Kouakanou, Léonce / Sun, Grace / Oliver-Cervantes, Cheryl / Georges, Joseph / Aftabizadeh, Maryam / Forman, Stephen / Priceman, Saul / Ressler, Julie / Arvanitis, Leonidas / Cotter, Jennifer / D'Apuzzo, Massimo / Tamrazi, Benita / Badie, Behnam / Davidson, Tom / Banovich, Nicholas / Brown, Christine

Research square

2023

Abstract: Outcomes for pediatric brain tumor patients remain poor, and there is optimism that chimeric antigen receptor (CAR) T cell therapy can improve prognosis. Here, we present interim results from the first six pediatric patients treated on an ongoing phase I ...

Abstract	Outcomes for pediatric brain tumor patients remain poor, and there is optimism that chimeric antigen receptor (CAR) T cell therapy can improve prognosis. Here, we present interim results from the first six pediatric patients treated on an ongoing phase I clinical trial (NCT04510051) of IL13BBζ-CAR T cells delivered weekly into the lateral cerebral ventricles, identifying clonal expansion of endogenous CAR-negative CD8
Language	English
Publishing date	2023-10-23
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3454977/v1
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Article ; Online: Integrin α6 signaling induces STAT3-TET3-mediated hydroxymethylation of genes critical for maintenance of glioma stem cells.

Herrmann, Andreas / Lahtz, Christoph / Song, Jieun / Aftabizadeh, Maryam / Cherryholmes, Gregory A / Xin, Hong / Adamus, Tomasz / Lee, Heehyoung / Grunert, David / Armstrong, Brian / Chu, Peiguo / Brown, Christine / Lim, Michael / Forman, Stephen / Yu, Hua

Oncogene

2019 Volume 39, Issue 10, Page(s) 2156–2169

Abstract: Both the extracellular matrix (ECM) and DNA epigenetic regulation are critical for maintaining stem cell phenotype and cancer progression. Whether and how ECM regulates epigenetic alterations to influence cancer stem cells (CSCs) remain to be explored. ... ...

Abstract	Both the extracellular matrix (ECM) and DNA epigenetic regulation are critical for maintaining stem cell phenotype and cancer progression. Whether and how ECM regulates epigenetic alterations to influence cancer stem cells (CSCs) remain to be explored. Here we report that ECM through laminin-integrin α6 upregulates ten-eleven translocation enzyme 3 (TET3) dioxygenase. TET3 in turn mediates DNA cytosine 5'-hydroxymethylation (5hmC) and upregulates genes critical for maintenance of glioma stem cells (GSCs). Activating integrin α6-FAK pathway increases STAT3 activity, TET3 expression and 5hmC levels in GSCs. Moreover, targeting STAT3 disrupts integrin α6-FAK signaling and inhibits TET3
MeSH term(s)	5-Methylcytosine ; Animals ; Cell Line ; DNA Methylation ; Dioxygenases/genetics ; Dioxygenases/metabolism ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Glioma/enzymology ; Glioma/genetics ; Glioma/metabolism ; Humans ; Integrin alpha6/metabolism ; Male ; Mice, Nude ; Neoplastic Stem Cells/enzymology ; Neoplastic Stem Cells/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Integrin alpha6 ; STAT3 Transcription Factor ; STAT3 protein, human ; 5-Methylcytosine (6R795CQT4H) ; TET3 protein, human (EC 1.-) ; Dioxygenases (EC 1.13.11.-)
Language	English
Publishing date	2019-12-09
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/s41388-019-1134-6
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Zs.A 2218: Show issues

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Article ; Online: STAT3 Activation-Induced Fatty Acid Oxidation in CD8

Cell metabolism

2019 Volume 31, Issue 1, Page(s) 148–161.e5

Abstract: Although obesity is known to be critical for cancer development, how obesity negatively impacts antitumor immune responses remains largely unknown. Here, we show that increased fatty acid oxidation (FAO) driven by activated STAT3 in ... ...

Abstract	Although obesity is known to be critical for cancer development, how obesity negatively impacts antitumor immune responses remains largely unknown. Here, we show that increased fatty acid oxidation (FAO) driven by activated STAT3 in CD8
MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Breast Neoplasms/immunology ; Breast Neoplasms/metabolism ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Carcinogenesis/genetics ; Carcinogenesis/immunology ; Carcinogenesis/metabolism ; Cell Line ; Cell Proliferation/genetics ; Chromatin Immunoprecipitation ; Fatty Acids/metabolism ; Female ; Glycolysis/genetics ; Glycolysis/physiology ; Humans ; Interferon-gamma/metabolism ; Leptin/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Obesity/immunology ; Obesity/metabolism ; Oxidation-Reduction/drug effects ; Programmed Cell Death 1 Receptor/metabolism ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism
Chemical Substances	Fatty Acids ; Leptin ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; STAT3 Transcription Factor ; STAT3 protein, human ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2019-11-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2019.10.013
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