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Article ; Online: Autophagy inhibition improves anti-cancer drugs

Fitzwalter, Brent E / Thorburn, Andrew

2018 Volume 9, Issue 39, Page(s) 25384–25385

Language	English
Publishing date	2018-05-22
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.25366
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Article ; Online: FOXO3 links autophagy to apoptosis.

Fitzwalter, Brent E / Thorburn, Andrew

Autophagy

2018 Volume 14, Issue 8, Page(s) 1467–1468

Abstract: The molecular machinery linking macroautophagy (autophagy hereafter) to apoptosis is still being elucidated. A recent study found that the transcription factor FOXO3/FOXO3A (forkhead box O3), which regulates autophagy, is itself regulated by basal ... ...

Abstract	The molecular machinery linking macroautophagy (autophagy hereafter) to apoptosis is still being elucidated. A recent study found that the transcription factor FOXO3/FOXO3A (forkhead box O3), which regulates autophagy, is itself regulated by basal autophagy to determine apoptosis sensitivity. Autophagy inhibition confers cell sensitivity to anti-cancer agents, and this effect is explained by the ability of FOXO3 to transactivate the pro-apoptotic gene BBC3/PUMA. Here, we discuss the possibility that FOXO3 acts as a cell surveillance mechanism to correct autophagy perturbations (i.e., autophagy inhibition), and confers apoptosis sensitization if this autophagy imbalance is not rectified.
MeSH term(s)	Apoptosis ; Autophagy ; Forkhead Box Protein O3/genetics ; Gene Expression Regulation
Chemical Substances	Forkhead Box Protein O3
Language	English
Publishing date	2018-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2018.1475819
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Zs.A 6741: Show issues

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Article ; Online: A caspase-independent way to kill cancer cells.

Fitzwalter, Brent E / Thorburn, Andrew

Nature cell biology

2017 Volume 19, Issue 9, Page(s) 1014–1015

Abstract: Cancer treatments often focus on killing tumour cells through apoptosis, which is thought to typically require mitochondrial outer membrane permeabilization (MOMP) and subsequent caspase activation. A study now shows that MOMP can trigger TNF-dependent, ... ...

Abstract	Cancer treatments often focus on killing tumour cells through apoptosis, which is thought to typically require mitochondrial outer membrane permeabilization (MOMP) and subsequent caspase activation. A study now shows that MOMP can trigger TNF-dependent, but caspase-independent cell death, suggesting a different approach to improve cancer therapy.
MeSH term(s)	Apoptosis ; Caspases ; Humans ; Mitochondria ; Mitochondrial Membranes
Chemical Substances	Caspases (EC 3.4.22.-)
Language	English
Publishing date	2017-08-31
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb3604
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Zs.A 5169: 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 12: Show issues

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Article ; Online: Recent insights into cell death and autophagy.

Fitzwalter, Brent E / Thorburn, Andrew

The FEBS journal

2015 Volume 282, Issue 22, Page(s) 4279–4288

Abstract: Macroautophagy (hereafter autophagy) is an evolutionarily-ancient mechanism by which cellular material is delivered to lysosomes for degradation. Autophagy and cell death are intimately linked. For example, both processes often use the same molecular ... ...

Abstract	Macroautophagy (hereafter autophagy) is an evolutionarily-ancient mechanism by which cellular material is delivered to lysosomes for degradation. Autophagy and cell death are intimately linked. For example, both processes often use the same molecular machinery and recent work suggests that autophagy has great influence over a cell's decision to live or die. However, this decision-making is complicated by the fact that the role of autophagy in determining whether a cell should live or die goes both ways: autophagy inhibition can result in more or less cell death depending on the death stimulus, cell type or context. Autophagy may also differentially affect different types of cell death. In the present review, we discuss the recent literature that helps make sense of this apparently inconsistent role of autophagy in influencing a cell to live or die.
MeSH term(s)	Animals ; Apoptosis/physiology ; Autophagy/physiology ; Humans ; Necrosis ; Receptor-Interacting Protein Serine-Threonine Kinases/physiology ; Receptors, Tumor Necrosis Factor, Type I/physiology ; ras Proteins/physiology
Chemical Substances	Receptors, Tumor Necrosis Factor, Type I ; RIPK1 protein, human (EC 2.7.11.1) ; RIPK3 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2015-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.13515
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Zs.A 260: Show issues

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Article ; Online: Single-cell dissection of the human motor and prefrontal cortices in ALS and FTLD.

Cell

2024 Volume 187, Issue 8, Page(s) 1971–1989.e16

Abstract: Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) share many clinical, pathological, and genetic features, but a detailed understanding of their associated transcriptional alterations across vulnerable cortical cell types ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) share many clinical, pathological, and genetic features, but a detailed understanding of their associated transcriptional alterations across vulnerable cortical cell types is lacking. Here, we report a high-resolution, comparative single-cell molecular atlas of the human primary motor and dorsolateral prefrontal cortices and their transcriptional alterations in sporadic and familial ALS and FTLD. By integrating transcriptional and genetic information, we identify known and previously unidentified vulnerable populations in cortical layer 5 and show that ALS- and FTLD-implicated motor and spindle neurons possess a virtually indistinguishable molecular identity. We implicate potential disease mechanisms affecting these cell types as well as non-neuronal drivers of pathogenesis. Finally, we show that neuron loss in cortical layer 5 tracks more closely with transcriptional identity rather than cellular morphology and extends beyond previously reported vulnerable cell types.
MeSH term(s)	Animals ; Humans ; Mice ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Frontotemporal Dementia/genetics ; Frontotemporal Lobar Degeneration/genetics ; Frontotemporal Lobar Degeneration/metabolism ; Frontotemporal Lobar Degeneration/pathology ; Gene Expression Profiling ; Neurons/metabolism ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/pathology ; Single-Cell Gene Expression Analysis
Language	English
Publishing date	2024-03-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2024.02.031
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: Cancer Cells Upregulate NRF2 Signaling to Adapt to Autophagy Inhibition.

Towers, Christina G / Fitzwalter, Brent E / Regan, Daniel / Goodspeed, Andrew / Morgan, Michael J / Liu, Chang-Wei / Gustafson, Daniel L / Thorburn, Andrew

Developmental cell

2019 Volume 50, Issue 6, Page(s) 690–703.e6

Abstract: While autophagy is thought to be an essential process in some cancer cells, it is unknown if or how such cancer cells can circumvent autophagy inhibition. To address this, we developed a CRISPR/Cas9 assay with dynamic live-cell imaging to measure acute ... ...

Abstract	While autophagy is thought to be an essential process in some cancer cells, it is unknown if or how such cancer cells can circumvent autophagy inhibition. To address this, we developed a CRISPR/Cas9 assay with dynamic live-cell imaging to measure acute effects of knockout (KO) of autophagy genes compared to known essential and non-essential genes. In some cancer cells, autophagy is as essential for cancer cell growth as mRNA transcription or translation or DNA replication. However, even these highly autophagy-dependent cancer cells evolve to circumvent loss of autophagy by upregulating NRF2, which is necessary and sufficient for autophagy-dependent cells to circumvent ATG7 KO and maintain protein homeostasis. Importantly, however, this adaptation increases susceptibly to proteasome inhibitors. These studies identify a common mechanism of acquired resistance to autophagy inhibition and show that selection to avoid tumor cell dependency on autophagy creates new, potentially actionable cancer cell susceptibilities.
MeSH term(s)	Adaptation, Physiological/drug effects ; Autophagy/drug effects ; Autophagy-Related Protein 7/metabolism ; CRISPR-Cas Systems/genetics ; Cell Line, Tumor ; Cell Survival/drug effects ; Clone Cells ; Gene Knockout Techniques ; Genes, Essential ; Humans ; NF-E2-Related Factor 2/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors/pharmacology ; Ribonucleoproteins/metabolism ; Signal Transduction/drug effects ; Up-Regulation/drug effects
Chemical Substances	NF-E2-Related Factor 2 ; Proteasome Inhibitors ; Ribonucleoproteins ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
Language	English
Publishing date	2019-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2019.07.010
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Zs.A 5742: 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 76: Show issues

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Article ; Online: Effect of early-stage autophagy inhibition in BRAF

Zahedi, Shadi / Fitzwalter, Brent E / Morin, Andrew / Grob, Sydney / Desmarais, Michele / Nellan, Anandani / Green, Adam L / Vibhakar, Rajeev / Hankinson, Todd C / Foreman, Nicholas K / Mulcahy Levy, Jean M

Cell death & disease

2019 Volume 10, Issue 9, Page(s) 679

Abstract: Autophagy is a multistage process. Progress within the field has led to the development of agents targeting both early (initiation) and late (fusion) stages of this process. The specific stage of autophagy targeted may influence cancer treatment outcomes. ...

Abstract	Autophagy is a multistage process. Progress within the field has led to the development of agents targeting both early (initiation) and late (fusion) stages of this process. The specific stage of autophagy targeted may influence cancer treatment outcomes. We have previously shown that central nervous system (CNS) tumors with the BRAF
MeSH term(s)	Aminopyridines/pharmacology ; Autophagy/drug effects ; Autophagy/genetics ; Benzamides/pharmacology ; Blotting, Western ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; Central Nervous System Neoplasms/genetics ; Central Nervous System Neoplasms/metabolism ; Flow Cytometry ; Humans ; Mutation/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Pyrimidines/pharmacology
Chemical Substances	1-((2-((2-chloropyridin-4yl)amino)-4'-(cyclopropylmethyl)-(4,5'-bipyrimidin)-2'-yl)amino)-2-methylpropan-2-ol ; Aminopyridines ; Benzamides ; Pyrimidines ; SBI-0206965 ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2019-09-12
Publishing country	England
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	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-019-1880-y
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Article ; Online: Metastatic cells are preferentially vulnerable to lysosomal inhibition.

Morgan, Michael J / Fitzwalter, Brent E / Owens, Charles R / Powers, Rani K / Sottnik, Joseph L / Gamez, Graciela / Costello, James C / Theodorescu, Dan / Thorburn, Andrew

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 36, Page(s) E8479–E8488

Abstract: Molecular alterations that confer phenotypic advantages to tumors can also expose specific therapeutic vulnerabilities. To search for potential treatments that would selectively affect metastatic cells, we examined the sensitivity of lineage-related ... ...

Abstract	Molecular alterations that confer phenotypic advantages to tumors can also expose specific therapeutic vulnerabilities. To search for potential treatments that would selectively affect metastatic cells, we examined the sensitivity of lineage-related human bladder cancer cell lines with different lung colonization abilities to chloroquine (CQ) or bafilomycin A
MeSH term(s)	Animals ; Cell Line, Tumor ; Chloroquine/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Inhibitor of Differentiation Proteins/biosynthesis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Lung Neoplasms/secondary ; Lysosomes/metabolism ; Lysosomes/pathology ; Macrolides/pharmacology ; Mice ; Neoplasm Metastasis ; Neoplasm Proteins/biosynthesis ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/metabolism ; Urinary Bladder Neoplasms/pathology
Chemical Substances	ID4 protein, human ; Inhibitor of Differentiation Proteins ; Macrolides ; Neoplasm Proteins ; Chloroquine (886U3H6UFF) ; bafilomycin A1 (88899-55-2)
Language	English
Publishing date	2018-08-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1706526115
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Zs.A 1148: Show issues

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Article ; Online: Autophagy Inhibition Mediates Apoptosis Sensitization in Cancer Therapy by Relieving FOXO3a Turnover.

Fitzwalter, Brent E / Towers, Christina G / Sullivan, Kelly D / Andrysik, Zdenek / Hoh, Maria / Ludwig, Michael / O'Prey, Jim / Ryan, Kevin M / Espinosa, Joaquin M / Morgan, Michael J / Thorburn, Andrew

Developmental cell

2018 Volume 44, Issue 5, Page(s) 555–565.e3

Abstract: Macroautophagy (autophagy) is intimately linked with cell death and allows cells to evade apoptosis. This has prompted clinical trials to combine autophagy inhibitors with other drugs with the aim of increasing the likelihood of cancer cells dying. ... ...

Abstract	Macroautophagy (autophagy) is intimately linked with cell death and allows cells to evade apoptosis. This has prompted clinical trials to combine autophagy inhibitors with other drugs with the aim of increasing the likelihood of cancer cells dying. However, the molecular basis for such effects is unknown. Here, we describe a transcriptional mechanism that connects autophagy to apoptosis. The autophagy-regulating transcription factor, FOXO3a, is itself turned over by basal autophagy creating a potential feedback loop. Increased FOXO3a upon autophagy inhibition stimulates transcription of the pro-apoptotic BBC3/PUMA gene to cause apoptosis sensitization. This mechanism explains how autophagy inhibition can sensitize tumor cells to chemotherapy drugs and allows an autophagy inhibitor to change the action of an MDM2-targeted drug from growth inhibition to apoptosis, reducing tumor burden in vivo. Thus, a link between two processes mediated via a single transcription factor binding site in the genome can be leveraged to improve anti-cancer therapies.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Autophagy/drug effects ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Female ; Forkhead Box Protein O3/genetics ; Forkhead Box Protein O3/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Tumor Cells, Cultured
Chemical Substances	Antineoplastic Agents ; Apoptosis Regulatory Proteins ; BBC3 protein, human ; FOXO3 protein, human ; Forkhead Box Protein O3 ; Proto-Oncogene Proteins
Language	English
Publishing date	2018-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2018.02.014
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Zs.A 5742: 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 76: Show issues

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Article ; Online: ZZ-dependent regulation of p62/SQSTM1 in autophagy.

Zhang, Yi / Mun, Su Ran / Linares, Juan F / Ahn, JaeWoo / Towers, Christina G / Ji, Chang Hoon / Fitzwalter, Brent E / Holden, Michael R / Mi, Wenyi / Shi, Xiaobing / Moscat, Jorge / Thorburn, Andrew / Diaz-Meco, Maria T / Kwon, Yong Tae / Kutateladze, Tatiana G

Nature communications

2018 Volume 9, Issue 1, Page(s) 4373

Abstract: Autophagic receptor p62 is a critical mediator of cell detoxification, stress response, and metabolic programs and is commonly deregulated in human diseases. The diverse functions of p62 arise from its ability to interact with a large set of ligands, ... ...

Abstract	Autophagic receptor p62 is a critical mediator of cell detoxification, stress response, and metabolic programs and is commonly deregulated in human diseases. The diverse functions of p62 arise from its ability to interact with a large set of ligands, such as arginylated (Nt-R) substrates. Here, we describe the structural mechanism for selective recognition of Nt-R by the ZZ domain of p62 (p62
MeSH term(s)	Autophagy/genetics ; Autophagy/physiology ; Cell Line ; Crystallography, X-Ray ; Flow Cytometry ; HEK293 Cells ; Humans ; Immunohistochemistry ; Magnetic Resonance Spectroscopy ; Mechanistic Target of Rapamycin Complex 1/genetics ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Protein Binding ; Sequestosome-1 Protein/genetics ; Sequestosome-1 Protein/metabolism ; Signal Transduction ; Spectrometry, Fluorescence
Chemical Substances	SQSTM1 protein, human ; Sequestosome-1 Protein ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2018-10-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-06878-8
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