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Article ; Online: Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm.

Moscat, Jorge / Cuervo, Ana Maria / Diaz-Meco, Maria T

2021 Volume 18, Issue 1, Page(s) 226–227

Abstract: The mechanisms controlling immunosurveillance and immunoevasion often operate simultaneously to the triggering of the oncogenic signaling that results in tumor initiation. The resolution of the balance between anti-cancer immune responses and pro- ... ...

Abstract	The mechanisms controlling immunosurveillance and immunoevasion often operate simultaneously to the triggering of the oncogenic signaling that results in tumor initiation. The resolution of the balance between anti-cancer immune responses and pro-tumorigenic pathways determines if a tumor cell survives and can remodel the microenvironment to reinforce immunosuppression or is eliminated by the immune system. Cancer cells must endure a toxic and metabolically challenging milieu. In its various forms, autophagy provides a way for transformed cells to survive by promoting catabolism and detoxification. Mounting evidence suggests that the boundaries between cancer immunity and mitogenic and metabolic programs are diffuse, with the same molecules likely serving several diverse roles in immunity and metabolism during tumor initiation and progression. Our recent data provide mechanistic detail and functional relevance of a new paradigm whereby the same signaling elements control immunity and autophagy in cancer.
MeSH term(s)	Autophagy/physiology ; Carcinogenesis ; Cell Transformation, Neoplastic ; Humans ; Interferons ; Isoenzymes/metabolism ; Monitoring, Immunologic ; Neoplasms/metabolism ; Protein Kinase C/metabolism ; Protein Serine-Threonine Kinases ; Signal Transduction ; Tumor Microenvironment
Chemical Substances	Isoenzymes ; Interferons (9008-11-1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ulk2 protein, human (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13) ; protein kinase C lambda (EC 2.7.11.13)
Language	English
Publishing date	2021-12-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2021.1991192
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Zs.A 6741: Show issues

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Article ; Online: Protein kinase Cλ/ι in cancer: a contextual balance of time and signals.

Moscat, Jorge / Linares, Juan F / Duran, Angeles / Diaz-Meco, Maria T

Trends in cell biology

2022 Volume 32, Issue 12, Page(s) 1023–1034

Abstract: Nononcogenic cancer drivers often impinge on complex signals that create new addictions and vulnerabilities. Protein kinase Cλ/ι (PKCλ/ι) suppresses tumorigenesis by blocking metabolic pathways that regulate fuel oxidation and create building blocks for ... ...

Abstract	Nononcogenic cancer drivers often impinge on complex signals that create new addictions and vulnerabilities. Protein kinase Cλ/ι (PKCλ/ι) suppresses tumorigenesis by blocking metabolic pathways that regulate fuel oxidation and create building blocks for the epigenetic control of cell differentiation. Reduced levels of PKCλ/ι unleash these pathways to promote tumorigenesis, but the simultaneous activation of the STING-driven interferon cascade prevents tumor initiation by triggering immunosurveillance mechanisms. However, depending on the context of other signaling pathways, such as WNT/β-catenin or PKCζ, and timing, PKCλ/ι deletion can promote or inhibit tumorigenesis. In this review, we discuss in detail the molecular and cellular underpinnings of PKCλ/ι functions in cancer with the perspective of the crosstalk between metabolism and inflammation in the tumor microenvironment.
MeSH term(s)	Humans ; Isoenzymes/metabolism ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Signal Transduction/physiology ; Neoplasms/genetics ; Cell Transformation, Neoplastic/pathology ; Tumor Microenvironment
Chemical Substances	Isoenzymes ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2022-04-29
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	30122-x
ISSN	1879-3088 ; 0962-8924
ISSN (online)	1879-3088
ISSN	0962-8924
DOI	10.1016/j.tcb.2022.04.002
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Zs.A 3410: 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: Sessile serrated lesions with dysplasia: is it possible to nip them in the bud?

Utsumi, Takahiro / Yamada, Yosuke / Diaz-Meco, Maria Teresa / Moscat, Jorge / Nakanishi, Yuki

Journal of gastroenterology

2023 Volume 58, Issue 8, Page(s) 705–717

Abstract: The serrated neoplasia pathway constitutes an "alternative route" to colorectal cancer (CRC), and sessile serrated lesions with dysplasia (SSLDs) are an intermediate step between sessile serrated lesions (SSLs) and invasive CRC in this pathway. While ... ...

Abstract	The serrated neoplasia pathway constitutes an "alternative route" to colorectal cancer (CRC), and sessile serrated lesions with dysplasia (SSLDs) are an intermediate step between sessile serrated lesions (SSLs) and invasive CRC in this pathway. While SSLs show indolent growth before becoming dysplastic (> 10-15 years), SSLDs are considered to rapidly progress to either immunogenic microsatellite instable-high (MSI-H) CRC (presumably 75% of cases) or mesenchymal microsatellite stable (MSS) CRC. Their flat shapes and the relatively short window of this intermediate state make it difficult to detect and diagnose SSLDs; thus, these lesions are potent precursors of post-colonoscopy/interval cancers. Confusing terminology and the lack of longitudinal observation data of serrated polyps have hampered the accumulation of knowledge about SSLDs; however, a growing body of evidence has started to clarify their characteristics and biology. Together with recent efforts to incorporate terminology, histological studies of SSLDs have identified distinct dysplastic patterns and revealed alterations in the tumor microenvironment (TME). Molecular studies at the single-cell level have identified distinct gene alterations in both the epithelium and the TME. Mouse serrated tumor models have demonstrated the importance of TME in disease progression. Advances in colonoscopy provide clues to distinguish pre-malignant from non-malignant-SSLs. Recent progress in all aspects of the field has enhanced our understanding of the biology of SSLDs. The aim of this review article was to assess the current knowledge of SSLDs and highlight their clinical implications.
MeSH term(s)	Animals ; Mice ; Colonic Polyps/genetics ; Colonic Polyps/pathology ; Colonic Neoplasms ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Colonoscopy ; Disease Progression ; Tumor Microenvironment
Language	English
Publishing date	2023-05-23
Publishing country	Japan
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1186495-3
ISSN	1435-5922 ; 0944-1174
ISSN (online)	1435-5922
ISSN	0944-1174
DOI	10.1007/s00535-023-02003-9
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Zs.A 620: Show issues

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Article ; Online: The interplay between PRKCI/PKCλ/ι, SQSTM1/p62, and autophagy orchestrates the oxidative metabolic response that drives liver cancer.

Moscat, Jorge / Diaz-Meco, Maria T

Autophagy

2020 Volume 16, Issue 10, Page(s) 1915–1917

Abstract: Hepatocellular carcinoma (HCC) is the consequence of chronic liver damage caused by the excessive generation of reactive oxygen species (ROS). To mitigate the deleterious effects of ROS, cells activate the transcription factor NFE2L2/NRF2, which is ... ...

Abstract	Hepatocellular carcinoma (HCC) is the consequence of chronic liver damage caused by the excessive generation of reactive oxygen species (ROS). To mitigate the deleterious effects of ROS, cells activate the transcription factor NFE2L2/NRF2, which is constitutively degraded through its partner KEAP1. The inactivation of KEAP1 by ROS results in the upregulation of NFE2L2, which leads to the upregulation of critical detoxifying molecules that serve to keep ROS at tolerable levels in order to maintain cell viability. It is thought that this mechanism allows cells to accumulate mutations, which together with the additional pro-tumorigenic and pro-survival effects of NFE2L2 activation, promote cancer initiation and progression. Germane to this phenomenon is macroautophagy/autophagy, which under homeostatic conditions has also been proposed to serve as a detoxifying mechanism by clearing up toxic aggregates and damaged organelles. Our recent data establish a new paradigm for the role that autophagy plays in HCC development.
MeSH term(s)	Autophagy ; Carcinoma, Hepatocellular ; Humans ; Kelch-Like ECH-Associated Protein 1/metabolism ; Liver Neoplasms ; NF-E2-Related Factor 2/metabolism ; Oxidative Phosphorylation ; Oxidative Stress ; Sequestosome-1 Protein/metabolism
Chemical Substances	Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; SQSTM1 protein, human ; Sequestosome-1 Protein
Language	English
Publishing date	2020-07-25
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	10.1080/15548627.2020.1797290
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Zs.A 6741: Show issues

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Article ; Online: Air-liquid organotypic assays to investigate cellular crosstalk in the tumor microenvironment of cancer cells.

Cid-Diaz, Tania / Lodeiro, Andrea C / Duran, Angeles / Moscat, Jorge / Diaz-Meco, Maria T

STAR protocols

2022 Volume 3, Issue 3, Page(s) 101635

Abstract: Air-liquid organotypic culture models enable the study of the cellular crosstalk in the tumor microenvironment. This 3D assay recapitulates the tumor niche more faithfully than 2D culture systems and represents a versatile platform that can be easily ... ...

Abstract	Air-liquid organotypic culture models enable the study of the cellular crosstalk in the tumor microenvironment. This 3D assay recapitulates the tumor niche more faithfully than 2D culture systems and represents a versatile platform that can be easily adapted to different types of cancer cells, stromal components, or ECM composition. Here, we detail the steps to build an organotypic culture including the preparation of the organotypic structure, organotypic gels, cell seeding, gel casting, membrane processing, and image and data analysis. For complete details on the use and execution of this protocol, please refer to Linares et al. (2022).
MeSH term(s)	Cell Line, Tumor ; Neoplasms ; Tumor Microenvironment
Language	English
Publishing date	2022-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2022.101635
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Article ; Online: Whole-mount staining of mouse colorectal cancer organoids and fibroblast-organoid co-cultures.

Martinez-Ordoñez, Anxo / Cid-Diaz, Tania / Duran, Angeles / Han, Qixiu / Moscat, Jorge / Diaz-Meco, Maria T

STAR protocols

2023 Volume 4, Issue 2, Page(s) 102243

Abstract: Imaging organoid culture provides an excellent tool for studying complex diseases such as cancer. However, retaining the morphology of intact organoids for immunolabeling has been challenging. Here, we describe a protocol for immunofluorescence staining ... ...

Abstract	Imaging organoid culture provides an excellent tool for studying complex diseases such as cancer. However, retaining the morphology of intact organoids for immunolabeling has been challenging. Here, we describe a protocol for immunofluorescence staining in intact colorectal cancer organoids derived from mice. We also describe additional steps for co-culture with mouse fibroblasts to enable the study of interactions with other cellular components of the tissue microenvironment. For complete details on the use and execution of this protocol, please refer to Martinez-Ordoñez et al. (2023).
Language	English
Publishing date	2023-04-20
Publishing country	United States
Document type	Journal Article
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2023.102243
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Article ; Online: Serrated Colorectal Cancer: The Road Less Travelled?

Nakanishi, Yuki / Diaz-Meco, Maria T / Moscat, Jorge

Trends in cancer

2019 Volume 5, Issue 11, Page(s) 742–754

Abstract: Studies of colorectal cancer (CRC) originating through the conventional adenoma-carcinoma sequence have provided insight into the molecular mechanisms controlling its initiation and progression. Less is known about the alternative 'serrated' pathway, ... ...

Abstract	Studies of colorectal cancer (CRC) originating through the conventional adenoma-carcinoma sequence have provided insight into the molecular mechanisms controlling its initiation and progression. Less is known about the alternative 'serrated' pathway, which has been associated with BRAF mutation and microsatellite instability. Recent transcriptomics approaches to classify human CRC revealed that mesenchymal and/or desmoplastic features combined with an immunosuppressive microenvironment are key determinants of CRC with the poorest prognosis. Importantly, these aggressive CRCs harbor the characteristics of serrated tumors, suggesting that initiation through this alternative pathway determines how aggressive the CRC becomes. Here, we review recent evidence on how serrated carcinogenesis contributes to the subtype of CRC with the poorest prognosis.
MeSH term(s)	Adenoma/genetics ; Adenoma/metabolism ; Adenoma/pathology ; Animals ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/therapy ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Profiling ; Humans ; Mice ; Microsatellite Instability ; Mutation ; Neoplasms, Experimental/pathology
Language	English
Publishing date	2019-10-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2019.09.004
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Article ; Online: The macroenviromental control of cancer metabolism by p62.

Huang, Jianfeng / Diaz-Meco, Maria T / Moscat, Jorge

Cell cycle (Georgetown, Tex.)

2018 Volume 17, Issue 17, Page(s) 2110–2121

Abstract: Metabolic reprogramming is a hallmark of cancer, but most studies focus on the molecular alterations in cancer cells and much less is known on the role of cancer metabolism, from a holistic perspective, for tumor initiation and progression. Increasing ... ...

Abstract	Metabolic reprogramming is a hallmark of cancer, but most studies focus on the molecular alterations in cancer cells and much less is known on the role of cancer metabolism, from a holistic perspective, for tumor initiation and progression. Increasing epidemiological evidence highlights the tremendous impact that cancer progression has on the host metabolism, especially in cachexia. However, how this benefits the tumor still is not completely understood. Here we review current studies on fatty acid oxidation in tumor cells as a potential therapeutic target in cancer, and how the redistribution of lipids from fat reservoirs to the cancer cell in the micro- and macro-environment impacts tumorigenesis by helping the tumor fulfill its energetic demands at the expense of fat. In this context, we also discuss the critical role of the signaling adaptor p62/Sequestosome 1(SQSTM1) in adipocytes in mediating tumor-induced fat reprograming and the feedback of adipose tissue on tumor aggressiveness via osteopontin and its potential implications in obesity-promoted cancer and fat cachexia. Collectively these studies highlight the importance of the symbiotic collaboration between adipose tissue and tumor to modulate the cancer metabolic fitness.
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Carcinogenesis/metabolism ; Cell Transformation, Neoplastic/metabolism ; Humans ; Lipid Metabolism/physiology ; Neoplasms/metabolism ; RNA-Binding Proteins/metabolism
Chemical Substances	P62 protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2018-09-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2018.1520566
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Zs.A 5881: Show issues

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Article ; Online: S-Nitrosylation of p62 Inhibits Autophagic Flux to Promote α-Synuclein Secretion and Spread in Parkinson's Disease and Lewy Body Dementia.

Oh, Chang-Ki / Dolatabadi, Nima / Cieplak, Piotr / Diaz-Meco, Maria T / Moscat, Jorge / Nolan, John P / Nakamura, Tomohiro / Lipton, Stuart A

The Journal of neuroscience : the official journal of the Society for Neuroscience

2022 Volume 42, Issue 14, Page(s) 3011–3024

Abstract: Dysregulation of autophagic pathways leads to accumulation of abnormal proteins and damaged organelles in many neurodegenerative disorders, including Parkinson's disease (PD) and Lewy body dementia (LBD). Autophagy-related dysfunction may also trigger ... ...

Abstract	Dysregulation of autophagic pathways leads to accumulation of abnormal proteins and damaged organelles in many neurodegenerative disorders, including Parkinson's disease (PD) and Lewy body dementia (LBD). Autophagy-related dysfunction may also trigger secretion and spread of misfolded proteins, such as α-synuclein (α-syn), the major misfolded protein found in PD/LBD. However, the mechanism underlying these phenomena remains largely unknown. Here, we used cell-based models, including human induced pluripotent stem cell-derived neurons, CRISPR/Cas9 technology, and male transgenic PD/LBD mice, plus vetting in human postmortem brains (both male and female). We provide mechanistic insight into this pathologic pathway. We find that aberrant S-nitrosylation of the autophagic adaptor protein p62 causes inhibition of autophagic flux and intracellular buildup of misfolded proteins, with consequent secretion resulting in cell-to-cell spread. Thus, our data show that pathologic protein S-nitrosylation of p62 represents a critical factor not only for autophagic inhibition and demise of individual neurons, but also for α-syn release and spread of disease throughout the nervous system.
MeSH term(s)	Animals ; Autophagy ; Female ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Lewy Body Disease/metabolism ; Lewy Body Disease/pathology ; Male ; Mice ; Mice, Transgenic ; Neurons/metabolism ; Neurons/pathology ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Protein S/metabolism ; RNA-Binding Proteins/metabolism ; alpha-Synuclein/metabolism
Chemical Substances	P62 protein, human ; Protein S ; RNA-Binding Proteins ; alpha-Synuclein
Language	English
Publishing date	2022-02-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1508-21.2022
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Zs.A 1668: Show issues

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Article ; Online: The Dual Roles of the Atypical Protein Kinase Cs in Cancer.

Reina-Campos, Miguel / Diaz-Meco, Maria T / Moscat, Jorge

Cancer cell

2019 Volume 36, Issue 3, Page(s) 218–235

Abstract: Atypical protein kinase C (aPKC) isozymes, PKCλ/ι and PKCζ, are now considered fundamental regulators of tumorigenesis. However, the specific separation of functions that determine their different roles in cancer is still being unraveled. Both aPKCs have ...

Abstract	Atypical protein kinase C (aPKC) isozymes, PKCλ/ι and PKCζ, are now considered fundamental regulators of tumorigenesis. However, the specific separation of functions that determine their different roles in cancer is still being unraveled. Both aPKCs have pleiotropic context-dependent functions that can translate into tumor-promoter or -suppressive functions. Here, we review early and more recent literature to discuss how the different tumor types, and their microenvironments, might account for the selective signaling of each aPKC isotype. This is of clinical relevance because a better understanding of the roles of these kinases is essential for the design of new anti-cancer treatments.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Polarity/genetics ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Disease Models, Animal ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/genetics ; Isoenzymes/metabolism ; Mice, Transgenic ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogenes/genetics ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Tumor Microenvironment/genetics ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Antineoplastic Agents ; Isoenzymes ; Protein Kinase Inhibitors ; Tumor Suppressor Proteins ; protein kinase C zeta (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13) ; protein kinase C lambda (EC 2.7.11.13)
Language	English
Publishing date	2019-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2019.07.010
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Zs.MG 104: Show issues

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