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Article ; Online: Mitophagy in tumorigenesis and metastasis.

Poole, Logan P / Macleod, Kay F

Cellular and molecular life sciences : CMLS

2021 Volume 78, Issue 8, Page(s) 3817–3851

Abstract: Cells use mitophagy to remove dysfunctional or excess mitochondria, frequently in response to imposed stresses, such as hypoxia and nutrient deprivation. Mitochondrial cargo receptors (MCR) induced by these stresses target mitochondria to autophagosomes ... ...

Abstract	Cells use mitophagy to remove dysfunctional or excess mitochondria, frequently in response to imposed stresses, such as hypoxia and nutrient deprivation. Mitochondrial cargo receptors (MCR) induced by these stresses target mitochondria to autophagosomes through interaction with members of the LC3/GABARAP family. There are a growing number of these MCRs, including BNIP3, BNIP3L, FUNDC1, Bcl2-L-13, FKBP8, Prohibitin-2, and others, in addition to mitochondrial protein targets of PINK1/Parkin phospho-ubiquitination. There is also an emerging link between mitochondrial lipid signaling and mitophagy where ceramide, sphingosine-1-phosphate, and cardiolipin have all been shown to promote mitophagy. Here, we review the upstream signaling mechanisms that regulate mitophagy, including components of the mitochondrial fission machinery, AMPK, ATF4, FoxOs, Sirtuins, and mtDNA release, and address the significance of these pathways for stress responses in tumorigenesis and metastasis. In particular, we focus on how mitophagy modulators intersect with cell cycle control and survival pathways in cancer, including following ECM detachment and during cell migration and metastasis. Finally, we interrogate how mitophagy affects tissue atrophy during cancer cachexia and therapy responses in the clinic.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Dynamics ; Mitophagy ; Neoplasm Metastasis/pathology ; Neoplasms/metabolism ; Neoplasms/pathology
Language	English
Publishing date	2021-02-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03774-1
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Article: DISSECTING TUMOR TRANSCRIPTIONAL HETEROGENEITY FROM SINGLE-CELL RNA-SEQ DATA BY GENERALIZED BINARY COVARIANCE DECOMPOSITION.

Liu, Yusha / Carbonetto, Peter / Willwerscheid, Jason / Oakes, Scott A / Macleod, Kay F / Stephens, Matthew

bioRxiv : the preprint server for biology

2023

Abstract: Profiling tumors with single-cell RNA sequencing (scRNA-seq) has the potential to identify recurrent patterns of transcription variation related to cancer progression, and so produce new therapeutically-relevant insights. However, the presence of strong ... ...

Abstract	Profiling tumors with single-cell RNA sequencing (scRNA-seq) has the potential to identify recurrent patterns of transcription variation related to cancer progression, and so produce new therapeutically-relevant insights. However, the presence of strong inter-tumor heterogeneity often obscures more subtle patterns that are shared across tumors, some of which may characterize clinically-relevant disease subtypes. Here we introduce a new statistical method to address this problem. We show that this method can help decompose transcriptional heterogeneity into interpretable components - including patient-specific, dataset-specific and shared components relevant to disease subtypes - and that, in the presence of strong inter-tumor heterogeneity, our method can produce more interpretable results than existing widely-used methods. Applied to data from three studies on pancreatic cancer adenocarcinoma (PDAC), our method produces a refined characterization of existing tumor subtypes (e.g. classical vs basal), and identifies a new gene expression program (GEP) that is prognostic of poor survival independent of established prognostic factors such as tumor stage and subtype. The new GEP is enriched for genes involved in a variety of stress responses, and suggests a potentially important role for the integrated stress response in PDAC development and prognosis.
Language	English
Publishing date	2023-08-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.08.15.553436
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Article ; Online: Autophagy, cancer stem cells and drug resistance.

Smith, Alexandra G / Macleod, Kay F

The Journal of pathology

2019 Volume 247, Issue 5, Page(s) 708–718

Abstract: Autophagy is a cellular survival mechanism that is induced by cancer therapy, among other stresses, and frequently contributes to cancer cell survival during long periods of dormancy and the eventual outgrowth of metastatic disease. Autophagy degrades ... ...

Abstract	Autophagy is a cellular survival mechanism that is induced by cancer therapy, among other stresses, and frequently contributes to cancer cell survival during long periods of dormancy and the eventual outgrowth of metastatic disease. Autophagy degrades large cellular structures that, once broken down, contribute to cellular survival through the recycling of their constituent metabolites. However, the extent to which this fuel function of autophagy is key to its role in promoting stemness, dormancy and drug resistance remains to be determined. Other roles for autophagy in determining cell fate more directly through targeted degradation of key transcription factors, such as p53 and FoxO3A, or by enforcing a reversible quiescent growth arrest, are discussed in this review. This review also highlights the need to parse out the roles of different forms of selective autophagy in stemness, CD44 expression and dormancy that, for example, are increasingly being attributed explicitly to mitophagy. The clinical relevance of this work and how an increased understanding of functions of autophagy in stemness, dormancy and drug resistance could be manipulated for increased therapeutic benefit, including eliminating minimal residual disease and preventing metastasis, are discussed. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Autophagy/physiology ; Disease Models, Animal ; Drug Resistance, Neoplasm/physiology ; Humans ; Mice ; Neoplasms/drug therapy ; Neoplasms/physiopathology ; Neoplastic Stem Cells/physiology
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2019-02-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.5222
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Article: Autophagy and cancer cell metabolism.

Anderson, Cara M / Macleod, Kay F

International review of cell and molecular biology

2019 Volume 347, Page(s) 145–190

Abstract: Autophagy is an ancient catabolic process used by cells to clear excess or dysfunctional organelles and large subcellular structures and thus performs an important housekeeping role for the cell. Autophagy is acutely sensitive to nutrient availability ... ...

Abstract	Autophagy is an ancient catabolic process used by cells to clear excess or dysfunctional organelles and large subcellular structures and thus performs an important housekeeping role for the cell. Autophagy is acutely sensitive to nutrient availability and is upregulated at a transcriptional and posttranslational level in response to nutrient deprivation. This serves to promote turnover of cellular content and recycling of nutrients for continued growth and survival. While important for most normal tissues, tumor cells appear to be particularly dependent on autophagy for survival under ischemic or therapeutic stress, and in response to loss of matrix attachment; autophagy is upregulated markedly in cancers as they progress to malignancy. Ras-driven tumors appear to be particularly dependent on autophagy and thus inhibition of autophagy is being pursued as a productive clinical approach for such cancers. However, this enthusiasm needs to be offset against possible negative effects of autophagy inhibition on normal tissue function and on limiting antitumor immune responses. In addressing all of these topics, we focus in on understanding how autophagy is induced by nutrient stress, its role in recycling metabolites for growing tumors, how selective forms of autophagy, such as mitophagy and ribophagy contribute specifically to tumorigenesis, how autophagy in the tumor microenvironment and throughout the animal affects access of the tumor to nutrients, and finally how different oncogenic pathways may determine which tumors respond to autophagy inhibition and which ones will not.
MeSH term(s)	Animals ; Autophagy ; Cancer-Associated Fibroblasts/metabolism ; Carcinogenesis ; Genetic Therapy ; Humans ; Lipid Metabolism ; Microphthalmia-Associated Transcription Factor/metabolism ; Mitophagy ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Tumor Microenvironment ; ras Proteins/genetics ; ras Proteins/metabolism
Chemical Substances	Microphthalmia-Associated Transcription Factor ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2019-07-09
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2427220-6
ISSN	1937-6448 ; 0074-7696
ISSN	1937-6448 ; 0074-7696
DOI	10.1016/bs.ircmb.2019.06.002
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Article: Mitophagy in tumorigenesis and metastasis

Poole, Logan P / Macleod, Kay F

Cellular and molecular life sciences. 2021 Apr., v. 78, no. 8

2021

Abstract	Cells use mitophagy to remove dysfunctional or excess mitochondria, frequently in response to imposed stresses, such as hypoxia and nutrient deprivation. Mitochondrial cargo receptors (MCR) induced by these stresses target mitochondria to autophagosomes through interaction with members of the LC3/GABARAP family. There are a growing number of these MCRs, including BNIP3, BNIP3L, FUNDC1, Bcl2-L-13, FKBP8, Prohibitin-2, and others, in addition to mitochondrial protein targets of PINK1/Parkin phospho-ubiquitination. There is also an emerging link between mitochondrial lipid signaling and mitophagy where ceramide, sphingosine-1-phosphate, and cardiolipin have all been shown to promote mitophagy. Here, we review the upstream signaling mechanisms that regulate mitophagy, including components of the mitochondrial fission machinery, AMPK, ATF4, FoxOs, Sirtuins, and mtDNA release, and address the significance of these pathways for stress responses in tumorigenesis and metastasis. In particular, we focus on how mitophagy modulators intersect with cell cycle control and survival pathways in cancer, including following ECM detachment and during cell migration and metastasis. Finally, we interrogate how mitophagy affects tissue atrophy during cancer cachexia and therapy responses in the clinic.
Keywords	atrophy ; autophagosomes ; cachexia ; carcinogenesis ; cardiolipins ; cell cycle ; cell movement ; ceramides ; hypoxia ; metastasis ; mitochondria ; mitochondrial proteins ; mitophagy ; sirtuins ; therapeutics
Language	English
Dates of publication	2021-04
Size	p. 3817-3851.
Publishing place	Springer International Publishing
Document type	Article
Note	NAL-AP-2-clean ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03774-1
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Lipid droplet turnover at the lysosome inhibits growth of hepatocellular carcinoma in a BNIP3-dependent manner.

Berardi, Damian E / Bock-Hughes, Althea / Terry, Alexander R / Drake, Lauren E / Bozek, Grazyna / Macleod, Kay F

Science advances

2022 Volume 8, Issue 41, Page(s) eabo2510

Abstract: Hepatic steatosis is a major etiological factor in hepatocellular carcinoma (HCC), but factors causing lipid accumulation leading to HCC are not understood. We identify BNIP3 (a mitochondrial cargo receptor) as an HCC suppressor that mitigates against ... ...

Abstract	Hepatic steatosis is a major etiological factor in hepatocellular carcinoma (HCC), but factors causing lipid accumulation leading to HCC are not understood. We identify BNIP3 (a mitochondrial cargo receptor) as an HCC suppressor that mitigates against lipid accumulation to attenuate tumor cell growth. Targeted deletion of
Language	English
Publishing date	2022-10-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abo2510
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Article ; Online: ULK1 promotes mitophagy via phosphorylation and stabilization of BNIP3.

Poole, Logan P / Bock-Hughes, Althea / Berardi, Damian E / Macleod, Kay F

Scientific reports

2021 Volume 11, Issue 1, Page(s) 20526

Abstract: UNC51-like kinase-1 (ULK1) is the catalytic component of the autophagy pre-initiation complex that stimulates autophagy via phosphorylation of ATG14, BECLN1 and other autophagy proteins. ULK1 has also been shown to specifically promote mitophagy but the ... ...

Abstract	UNC51-like kinase-1 (ULK1) is the catalytic component of the autophagy pre-initiation complex that stimulates autophagy via phosphorylation of ATG14, BECLN1 and other autophagy proteins. ULK1 has also been shown to specifically promote mitophagy but the mechanistic basis of how has remained unclear. Here we show that ULK1 phosphorylates the BNIP3 mitochondrial cargo receptor on a critical serine residue (S17) adjacent to its amino terminal LIR motif. ULK1 similarly phosphorylates BNIP3L on S35. Phosphorylation of BNIP3 on S17 by ULK1 promotes interaction with LC3 and mitophagy. ULK1 interaction also promotes BNIP3 protein stability by limiting its turnover at the proteasome. The ability of ULK1 to regulate BNIP3 protein stability depends on an intact "BH3" domain and deletion of its "BH3" domain reduces BNIP3 turnover and increases BNIP3 protein levels independent of ULK1. In summary ULK1 promotes mitophagy by both stabilization of BNIP3 protein and via phosphorylation of S17 to stimulate interaction with LC3.
MeSH term(s)	Autophagy-Related Protein-1 Homolog/metabolism ; Cell Line, Tumor ; HEK293 Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/metabolism ; Mitophagy ; Phosphorylation ; Proteasome Endopeptidase Complex/metabolism ; Proto-Oncogene Proteins/metabolism ; Tumor Suppressor Proteins/metabolism
Chemical Substances	BNIP3 protein, human ; BNIP3L protein, human ; Intracellular Signaling Peptides and Proteins ; MAP1LC3B protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; Proto-Oncogene Proteins ; Tumor Suppressor Proteins ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; ULK1 protein, human (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2021-10-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-00170-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: In Brief: Mitophagy: mechanisms and role in human disease.

Springer, Maya Z / Macleod, Kay F

The Journal of pathology

2016 Volume 240, Issue 3, Page(s) 253–255

Abstract: Mitophagy is a selective form of macro-autophagy in which mitochondria are specifically targeted for autophagic degradation. Mitophagy plays an important role in cellular homeostasis by eliminating dysfunctional mitochondria and reducing mitochondrial ... ...

Abstract	Mitophagy is a selective form of macro-autophagy in which mitochondria are specifically targeted for autophagic degradation. Mitophagy plays an important role in cellular homeostasis by eliminating dysfunctional mitochondria and reducing mitochondrial mass as an adaptive response to stress. Cells execute mitophagy through several non-redundant mechanisms, including the PINK1/Parkin partnership, which modulates turnover of depolarized mitochondria, and stress-induced BNIP3, NIX, and FUNDC1 molecular adaptors, which interact directly with LC3 to promote mitophagy. These pathways are deregulated in human diseases, including cancer, neurodegeneration, metabolic disorders, muscle atrophy, ageing, and inflammation, reflecting the importance of mitophagy as a cellular housekeeping function. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
MeSH term(s)	Adaptation, Physiological ; Aging/genetics ; Aging/physiology ; Autophagy ; Homeostasis ; Humans ; Inflammation/genetics ; Inflammation/physiopathology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Metabolic Diseases/genetics ; Metabolic Diseases/physiopathology ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mitochondria/pathology ; Mitochondria/physiology ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Mitophagy/physiology ; Models, Biological ; Muscular Atrophy/genetics ; Muscular Atrophy/physiopathology ; Neoplasms/genetics ; Neoplasms/physiopathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/physiopathology ; Protein Interaction Maps ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Signal Transduction ; Stress, Physiological ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	BNIP3 protein, human ; BNIP3L protein, human ; FUNDC1 protein, human ; MAP1LC3A protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; Mitochondrial Proteins ; Proto-Oncogene Proteins ; Tumor Suppressor Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; parkin protein (EC 2.3.2.27)
Language	English
Publishing date	2016-09-29
Publishing country	England
Document type	Journal Article
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.4774
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Article ; Online: ULK1 promotes mitophagy via phosphorylation and stabilization of BNIP3

Logan P. Poole / Althea Bock-Hughes / Damian E. Berardi / Kay F. Macleod

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 15

Abstract: Abstract UNC51-like kinase-1 (ULK1) is the catalytic component of the autophagy pre-initiation complex that stimulates autophagy via phosphorylation of ATG14, BECLN1 and other autophagy proteins. ULK1 has also been shown to specifically promote mitophagy ...

Abstract	Abstract UNC51-like kinase-1 (ULK1) is the catalytic component of the autophagy pre-initiation complex that stimulates autophagy via phosphorylation of ATG14, BECLN1 and other autophagy proteins. ULK1 has also been shown to specifically promote mitophagy but the mechanistic basis of how has remained unclear. Here we show that ULK1 phosphorylates the BNIP3 mitochondrial cargo receptor on a critical serine residue (S17) adjacent to its amino terminal LIR motif. ULK1 similarly phosphorylates BNIP3L on S35. Phosphorylation of BNIP3 on S17 by ULK1 promotes interaction with LC3 and mitophagy. ULK1 interaction also promotes BNIP3 protein stability by limiting its turnover at the proteasome. The ability of ULK1 to regulate BNIP3 protein stability depends on an intact “BH3” domain and deletion of its “BH3” domain reduces BNIP3 turnover and increases BNIP3 protein levels independent of ULK1. In summary ULK1 promotes mitophagy by both stabilization of BNIP3 protein and via phosphorylation of S17 to stimulate interaction with LC3.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Functions of autophagy in the tumor microenvironment and cancer metastasis.

Mowers, Erin E / Sharifi, Marina N / Macleod, Kay F

The FEBS journal

2018 Volume 285, Issue 10, Page(s) 1751–1766

Abstract: Macro-autophagy is an ancient and highly conserved self-degradative process that plays a homeostatic role in normal cells by eliminating organelles, pathogens, and protein aggregates. Autophagy, as it is routinely referred to, also allows cells to ... ...

Abstract	Macro-autophagy is an ancient and highly conserved self-degradative process that plays a homeostatic role in normal cells by eliminating organelles, pathogens, and protein aggregates. Autophagy, as it is routinely referred to, also allows cells to maintain metabolic sufficiency and survive under conditions of nutrient stress by recycling the by-products of autophagic degradation, such as fatty acids, amino acids, and nucleotides. Tumor cells are more reliant than normal cells on autophagy for survival in part due to their rapid growth rate, altered metabolism, and nutrient-deprived growth environment. How this dependence of tumor cells on autophagy affects their progression to malignancy and metastatic disease is an area of increasing research focus. Here, we review recent work identifying critical functions for autophagy in tumor cell migration and invasion, tumor stem cell maintenance and therapy resistance, and cross-talk between tumor cells and their microenvironment.
MeSH term(s)	Autophagy/physiology ; Humans ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasms/pathology ; Neoplastic Stem Cells/pathology ; Tumor Microenvironment
Language	English
Publishing date	2018-02-01
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.14388
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