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Article ; Online: Autophagy cooperates with PDGFRA to support oncogenic growth signaling.

Simpson, Joanne E / Gammoh, Noor

2024 , Page(s) 1–2

Abstract: Macroautophagy (referred to as autophagy hereafter) is a highly conserved catabolic process which sequesters intracellular substrates for lysosomal degradation. Autophagy-related proteins have been shown to be involved in various aspects of tumor ... ...

Abstract	Macroautophagy (referred to as autophagy hereafter) is a highly conserved catabolic process which sequesters intracellular substrates for lysosomal degradation. Autophagy-related proteins have been shown to be involved in various aspects of tumor development by engaging with multiple cellular substrates. We recently uncovered a novel role for autophagy in regulating the signaling and levels of PDGFRA, a receptor tyrosine kinase amplified in several cancers. We discovered that PDGFRA can be targeted to autophagic degradation by binding the autophagy cargo receptor SQSTM1. Surprisingly, PDGFRA-mediated signaling is perturbed in the absence of autophagy despite enhanced receptor levels. We show that this is due to disrupted trafficking of the receptor to late endosomes where signaling activity persists. Conversely, prolonged autophagy inhibition results in a transcriptional downregulation of
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2024.2338572
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Article ; Online: The multifaceted functions of ATG16L1 in autophagy and related processes.

Gammoh, Noor

Journal of cell science

2020 Volume 133, Issue 20

Abstract: Autophagy requires the formation of membrane vesicles, known as autophagosomes, that engulf cellular cargoes and subsequently recruit lysosomal hydrolases for the degradation of their contents. A number of autophagy-related proteins act to mediate ... ...

Abstract	Autophagy requires the formation of membrane vesicles, known as autophagosomes, that engulf cellular cargoes and subsequently recruit lysosomal hydrolases for the degradation of their contents. A number of autophagy-related proteins act to mediate the
MeSH term(s)	Autophagosomes ; Autophagy/genetics ; Autophagy-Related Proteins/genetics ; Lysosomes
Chemical Substances	Autophagy-Related Proteins
Language	English
Publishing date	2020-10-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.249227
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Zs.A 1200: 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 14: Show issues

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Article ; Online: Autophagy and autophagy-related pathways in cancer.

Debnath, Jayanta / Gammoh, Noor / Ryan, Kevin M

Nature reviews. Molecular cell biology

2023 Volume 24, Issue 8, Page(s) 560–575

Abstract: Maintenance of protein homeostasis and organelle integrity and function is critical for cellular homeostasis and cell viability. Autophagy is the principal mechanism that mediates the delivery of various cellular cargoes to lysosomes for degradation and ... ...

Abstract	Maintenance of protein homeostasis and organelle integrity and function is critical for cellular homeostasis and cell viability. Autophagy is the principal mechanism that mediates the delivery of various cellular cargoes to lysosomes for degradation and recycling. A myriad of studies demonstrate important protective roles for autophagy against disease. However, in cancer, seemingly opposing roles of autophagy are observed in the prevention of early tumour development versus the maintenance and metabolic adaptation of established and metastasizing tumours. Recent studies have addressed not only the tumour cell intrinsic functions of autophagy, but also the roles of autophagy in the tumour microenvironment and associated immune cells. In addition, various autophagy-related pathways have been described, which are distinct from classical autophagy, that utilize parts of the autophagic machinery and can potentially contribute to malignant disease. Growing evidence on how autophagy and related processes affect cancer development and progression has helped guide efforts to design anticancer treatments based on inhibition or promotion of autophagy. In this Review, we discuss and dissect these different functions of autophagy and autophagy-related processes during tumour development, maintenance and progression. We outline recent findings regarding the role of these processes in both the tumour cells and the tumour microenvironment and describe advances in therapy aimed at autophagy processes in cancer.
MeSH term(s)	Humans ; Neoplasms/pathology ; Autophagy/physiology ; Lysosomes ; Tumor Microenvironment
Language	English
Publishing date	2023-03-02
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2031313-5
ISSN	1471-0080 ; 1471-0072
ISSN (online)	1471-0080
ISSN	1471-0072
DOI	10.1038/s41580-023-00585-z
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Zs.A 5446: 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: The impact of autophagy during the development and survival of glioblastoma.

Simpson, Joanne E / Gammoh, Noor

Open biology

2020 Volume 10, Issue 9, Page(s) 200184

Abstract: Glioblastoma is the most common and aggressive adult brain tumour, with poor median survival and limited treatment options. Following surgical resection and chemotherapy, recurrence of the disease is inevitable. Genomic studies have identified key ... ...

Abstract	Glioblastoma is the most common and aggressive adult brain tumour, with poor median survival and limited treatment options. Following surgical resection and chemotherapy, recurrence of the disease is inevitable. Genomic studies have identified key drivers of glioblastoma development, including amplifications of receptor tyrosine kinases, which drive tumour growth. To improve treatment, it is crucial to understand survival response processes in glioblastoma that fuel cell proliferation and promote resistance to treatment. One such process is autophagy, a catabolic pathway that delivers cellular components sequestered into vesicles for lysosomal degradation. Autophagy plays an important role in maintaining cellular homeostasis and is upregulated during stress conditions, such as limited nutrient and oxygen availability, and in response to anti-cancer therapy. Autophagy can also regulate pro-growth signalling and metabolic rewiring of cancer cells in order to support tumour growth. In this review, we will discuss our current understanding of how autophagy is implicated in glioblastoma development and survival. When appropriate, we will refer to findings derived from the role of autophagy in other cancer models and predict the outcome of manipulating autophagy during glioblastoma treatment.
MeSH term(s)	Animals ; Autophagy/genetics ; Autophagy/immunology ; Biomarkers, Tumor ; Brain Neoplasms/diagnosis ; Brain Neoplasms/etiology ; Brain Neoplasms/mortality ; Brain Neoplasms/therapy ; Cell Line ; Cell Transformation, Neoplastic ; Cells, Cultured ; Disease Management ; Disease Models, Animal ; Disease Susceptibility ; Gene Expression Regulation, Neoplastic ; Glioblastoma/diagnosis ; Glioblastoma/etiology ; Glioblastoma/mortality ; Glioblastoma/therapy ; Humans ; Immunomodulation ; Models, Biological ; Prognosis ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction ; Treatment Outcome
Chemical Substances	Biomarkers, Tumor ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2020-09-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2630944-0
ISSN	2046-2441 ; 2046-2441
ISSN (online)	2046-2441
ISSN	2046-2441
DOI	10.1098/rsob.200184
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Article ; Online: Autophagy Brings an END to Aberrant Endocytosis.

Makar, Agata N / Gammoh, Noor

Molecular cell

2020 Volume 80, Issue 5, Page(s) 758–759

Abstract: Wilfling et al. (2020) characterize a selective autophagy pathway in yeast for early clathrin-mediated endocytosis (CME) proteins facilitated by the phase separation of the CME protein, Ede1, which acts as an intrinsic autophagy receptor for the ... ...

Abstract	Wilfling et al. (2020) characterize a selective autophagy pathway in yeast for early clathrin-mediated endocytosis (CME) proteins facilitated by the phase separation of the CME protein, Ede1, which acts as an intrinsic autophagy receptor for the degradation of Ede1-dependent endocytic protein deposits (ENDs).
MeSH term(s)	Autophagy ; Clathrin ; Endocytosis ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics
Chemical Substances	Clathrin ; Saccharomyces cerevisiae Proteins
Language	English
Publishing date	2020-12-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.11.020
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Article: Autophagy Brings an END to Aberrant Endocytosis

Makar, Agata N. / Gammoh, Noor

Molecular cell. 2020 Dec. 03, v. 80, no. 5

2020

Abstract	Wilfling et al. (2020) characterize a selective autophagy pathway in yeast for early clathrin-mediated endocytosis (CME) proteins facilitated by the phase separation of the CME protein, Ede1, which acts as an intrinsic autophagy receptor for the degradation of Ede1-dependent endocytic protein deposits (ENDs).
Keywords	autophagy ; endocytosis ; separation ; yeasts
Language	English
Dates of publication	2020-1203
Size	p. 758-759.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2020.11.020
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Membrane targeting of core autophagy players during autophagosome biogenesis.

Dudley, Leo J / Makar, Agata N / Gammoh, Noor

The FEBS journal

2020 Volume 287, Issue 22, Page(s) 4806–4821

Abstract: Autophagosomes are vital organelles required to facilitate the lysosomal degradation of cytoplasmic cargo, thereby playing an important role in maintaining cellular homeostasis. A number of autophagy-related (ATG) protein complexes are recruited to the ... ...

Abstract	Autophagosomes are vital organelles required to facilitate the lysosomal degradation of cytoplasmic cargo, thereby playing an important role in maintaining cellular homeostasis. A number of autophagy-related (ATG) protein complexes are recruited to the site of autophagosome biogenesis where they act to facilitate membrane growth and maturation. Regulated recruitment of ATG complexes to autophagosomal membranes is essential for their autophagic activities and is required to ensure the efficient engulfment of cargo destined for lysosomal degradation. In this review, we discuss our current understanding of the spatiotemporal hierarchy between ATG proteins, examining the mechanisms underlying their recruitment to membranes. A particular focus is placed on the relevance of phosphatidylinositol 3-phosphate and the extent to which the core autophagy players are reliant on this lipid for their localisation to autophagic membranes. In addition, open questions and potential future research directions regarding the membrane recruitment and displacement of ATG proteins are discussed here.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy ; Autophagy-Related Proteins/metabolism ; Humans ; Intracellular Membranes/metabolism ; Lysosomes/metabolism ; Phagosomes/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Protein Binding
Chemical Substances	Autophagy-Related Proteins ; Phosphatidylinositol Phosphates ; phosphatidylinositol 3-phosphate
Language	English
Publishing date	2020-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.15334
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Zs.A 260: Show issues

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Article ; Online: Autophagy supports PDGFRA-dependent brain tumor development by enhancing oncogenic signaling.

Simpson, Joanne E / Muir, Morwenna T / Lee, Martin / Naughton, Catherine / Gilbert, Nick / Pollard, Steven M / Gammoh, Noor

Developmental cell

2023 Volume 59, Issue 2, Page(s) 228–243.e7

Abstract: Autophagy is a conserved cellular degradation process. While autophagy-related proteins were shown to influence the signaling and trafficking of some receptor tyrosine kinases, the relevance of this during cancer development is unclear. Here, we identify ...

Abstract	Autophagy is a conserved cellular degradation process. While autophagy-related proteins were shown to influence the signaling and trafficking of some receptor tyrosine kinases, the relevance of this during cancer development is unclear. Here, we identify a role for autophagy in regulating platelet-derived growth factor receptor alpha (PDGFRA) signaling and levels. We find that PDGFRA can be targeted for autophagic degradation through the activity of the autophagy cargo receptor p62. As a result, short-term autophagy inhibition leads to elevated levels of PDGFRA but an unexpected defect in PDGFA-mediated signaling due to perturbed receptor trafficking. Defective PDGFRA signaling led to its reduced levels during prolonged autophagy inhibition, suggesting a mechanism of adaptation. Importantly, PDGFA-driven gliomagenesis in mice was disrupted when autophagy was inhibited in a manner dependent on Pten status, thus highlighting a genotype-specific role for autophagy during tumorigenesis. In summary, our data provide a mechanism by which cells require autophagy to drive tumor formation.
MeSH term(s)	Mice ; Animals ; Signal Transduction ; Brain Neoplasms ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Platelet-Derived Growth Factor alpha/metabolism ; Autophagy
Chemical Substances	Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1)
Language	English
Publishing date	2023-12-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2023.11.023
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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: Targeting of early endosomes by autophagy facilitates EGFR recycling and signalling.

Fraser, Jane / Simpson, Joanne / Fontana, Rosa / Kishi-Itakura, Chieko / Ktistakis, Nicholas T / Gammoh, Noor

EMBO reports

2019 Volume 20, Issue 10, Page(s) e47734

Abstract: Despite recently uncovered connections between autophagy and the endocytic pathway, the role of autophagy in regulating endosomal function remains incompletely understood. Here, we find that the ablation of autophagy-essential players disrupts EGF- ... ...

Abstract	Despite recently uncovered connections between autophagy and the endocytic pathway, the role of autophagy in regulating endosomal function remains incompletely understood. Here, we find that the ablation of autophagy-essential players disrupts EGF-induced endocytic trafficking of EGFR. Cells lacking ATG7 or ATG16L1 exhibit increased levels of phosphatidylinositol-3-phosphate (PI(3)P), a key determinant of early endosome maturation. Increased PI(3)P levels are associated with an accumulation of EEA1-positive endosomes where EGFR trafficking is stalled. Aberrant early endosomes are recognised by the autophagy machinery in a TBK1- and Gal8-dependent manner and are delivered to LAMP2-positive lysosomes. Preventing this homeostatic regulation of early endosomes by autophagy reduces EGFR recycling to the plasma membrane and compromises downstream signalling and cell survival. Our findings uncover a novel role for the autophagy machinery in maintaining early endosome function and growth factor sensing.
MeSH term(s)	Animals ; Autophagy/drug effects ; Cell Line ; Cell Survival/drug effects ; Endocytosis/drug effects ; Endosomes/drug effects ; Endosomes/metabolism ; Epidermal Growth Factor/metabolism ; ErbB Receptors/metabolism ; Galectins/metabolism ; Humans ; Mice ; Monensin/pharmacology ; Phosphatidylinositol Phosphates/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Signal Transduction/drug effects ; rab GTP-Binding Proteins/metabolism
Chemical Substances	Galectins ; Phosphatidylinositol Phosphates ; phosphatidylinositol 3-phosphate ; Epidermal Growth Factor (62229-50-9) ; Monensin (906O0YJ6ZP) ; ErbB Receptors (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; rab11 protein (EC 3.6.1.-) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2019-08-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.201947734
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Zs.A 5433: 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: Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking.

Fraser, Jane / Cabodevilla, Ainara G / Simpson, Joanne / Gammoh, Noor

Essays in biochemistry

2017 Volume 61, Issue 6, Page(s) 597–607

Abstract: Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. ... ...

Abstract	Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking players are not direct drivers of cellular transformation, their activities are important in facilitating oncogenic pathways. One such pathway is the sensing of external stimuli and signalling through receptor tyrosine kinases (RTKs). The regulation of RTK activity by the endocytic pathway has been extensively studied. Compelling recent studies have begun to highlight the association between autophagy and RTK signalling. The influence of this interplay on cellular status and its relevance in disease settings will be discussed here.
MeSH term(s)	Animals ; Autophagy/genetics ; Autophagy/physiology ; Endocytosis/genetics ; Endocytosis/physiology ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction/genetics ; Signal Transduction/physiology
Chemical Substances	Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2017-12-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	1744-1358 ; 0071-1365
ISSN (online)	1744-1358
ISSN	0071-1365
DOI	10.1042/EBC20170091
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