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Article: Role of autophagy in cancer-associated fibroblast activation, signaling and metabolic reprograming.

Sari, Dyana / Gozuacik, Devrim / Akkoc, Yunus

Frontiers in cell and developmental biology

2024 Volume 11, Page(s) 1274682

Abstract: Tumors not only consist of cancerous cells, but they also harbor several normal-like cell types and non-cellular components. cancer-associated fibroblasts (CAFs) are one of these cellular components that are found predominantly in the tumor stroma. ... ...

Abstract	Tumors not only consist of cancerous cells, but they also harbor several normal-like cell types and non-cellular components. cancer-associated fibroblasts (CAFs) are one of these cellular components that are found predominantly in the tumor stroma. Autophagy is an intracellular degradation and quality control mechanism, and recent studies provided evidence that autophagy played a critical role in CAF formation, metabolic reprograming and tumor-stroma crosstalk. Therefore, shedding light on the autophagy and its role in CAF biology might help us better understand the roles of CAFs and the TME in cancer progression and may facilitate the exploitation of more efficient cancer diagnosis and treatment. Here, we provide an overview about the involvement of autophagy in CAF-related pathways, including transdifferentiation and activation of CAFs, and further discuss the implications of targeting tumor stroma as a treatment option.
Language	English
Publishing date	2024-01-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1274682
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Article ; Online: Role of autophagy in cancer-associated fibroblast activation, signaling and metabolic reprograming

Dyana Sari / Devrim Gozuacik / Yunus Akkoc

Frontiers in Cell and Developmental Biology, Vol

2024 Volume 11

Abstract	Tumors not only consist of cancerous cells, but they also harbor several normal-like cell types and non-cellular components. cancer-associated fibroblasts (CAFs) are one of these cellular components that are found predominantly in the tumor stroma. Autophagy is an intracellular degradation and quality control mechanism, and recent studies provided evidence that autophagy played a critical role in CAF formation, metabolic reprograming and tumor-stroma crosstalk. Therefore, shedding light on the autophagy and its role in CAF biology might help us better understand the roles of CAFs and the TME in cancer progression and may facilitate the exploitation of more efficient cancer diagnosis and treatment. Here, we provide an overview about the involvement of autophagy in CAF-related pathways, including transdifferentiation and activation of CAFs, and further discuss the implications of targeting tumor stroma as a treatment option.
Keywords	cancer-associated fibroblasts (CAFs) ; autophagy ; tumor microenvironment (TME) ; fibroblast transdifferentiation ; cancer ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Autophagy and Hepatic Tumor Microenvironment Associated Dormancy.

Akkoc, Yunus / Gozuacik, Devrim

Journal of gastrointestinal cancer

2021 Volume 52, Issue 4, Page(s) 1277–1293

Abstract: The goal of successful cancer treatment is targeting the eradication of cancer cells. Although surgical removal of the primary tumors and several rounds of chemo- and radiotherapy reduce the disease burden, in some cases, asymptomatic dormant cancer ... ...

Abstract	The goal of successful cancer treatment is targeting the eradication of cancer cells. Although surgical removal of the primary tumors and several rounds of chemo- and radiotherapy reduce the disease burden, in some cases, asymptomatic dormant cancer cells may still exist in the body. Dormant cells arise from the disseminated tumor cells (DTCs) from the primary lesion. DTCs escape from immune system and cancer therapy and reside at the secondary organ without showing no sign of proliferation. However, under some conditions. dormant cells can be re-activated and enter a proliferative state even after decades. As a stress response mechanism, autophagy may help the adaptation of DTCs at this futile foreign microenvironment and may control the survival and re-activation of dormant cells. Studies indicate that hepatic microenvironment serves a favorable condition for cancer cell dormancy. Although, no direct study was pointing out the role of autophagy in liver-assisted dormancy, involvement of autophagy in both liver microenvironment, health, and disease conditions has been indicated. Therefore, in this review article, we will summarize cancer dormancy and discuss the role and importance of autophagy and hepatic microenvironment in this context.
MeSH term(s)	Animals ; Autophagy/physiology ; Breast Neoplasms/metabolism ; Female ; Humans ; Liver Neoplasms/metabolism ; Liver Neoplasms/physiopathology ; Male ; Mice ; Neoplasm Metastasis/physiopathology ; Neoplasm, Residual/metabolism ; Tumor Microenvironment/physiology
Language	English
Publishing date	2021-12-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2452514-5
ISSN	1941-6636 ; 1559-0739 ; 1941-6628 ; 1537-3649
ISSN (online)	1941-6636 ; 1559-0739
ISSN	1941-6628 ; 1537-3649
DOI	10.1007/s12029-021-00774-z
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Zs.A 2184: Show issues

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Article ; Online: Cancer Recurrence and Omics: Metabolic Signatures of Cancer Dormancy Revealed by Transcriptome Mapping of Genome-Scale Networks.

Kutay, Merve / Gozuacik, Devrim / Çakır, Tunahan

Omics : a journal of integrative biology

2022 Volume 26, Issue 5, Page(s) 270–279

Abstract: A major problem in medicine and oncology is cancer recurrence through the activation of dormant cancer cells. A system scale examination of metabolic dysregulations associated with the cancer dormancy offers promise for the discovery of novel molecular ... ...

Abstract	A major problem in medicine and oncology is cancer recurrence through the activation of dormant cancer cells. A system scale examination of metabolic dysregulations associated with the cancer dormancy offers promise for the discovery of novel molecular targets for cancer precision medicine, and importantly, for the prevention of cancer recurrence. In this study, we mapped the total mRNA sequencing-based transcriptomic data from dormant cancer cell lines and nondormant cancer controls onto a human genome-scale metabolic network by using a graph-based approach, and two mass balance-based approaches with one based on reaction activity/inactivity and the other one on flux changes. The gene expression datasets were accessed from Gene Expression Omnibus (GSE83142 and GSE114012). This analysis included two diverse cancer types, a liquid and a solid cancer, namely, acute lymphoblastic leukemia and colorectal cancer. For the dormant cancer state, we observed changes in major adenosine triphosphate-producing pathways, including the citric acid cycle, oxidative phosphorylation, and glycolysis/gluconeogenesis, indicating a reprogramming in the metabolism of dormant cells away from Warburg-based energy metabolism. All three computational approaches unanimously predicted that folate metabolism, pyruvate metabolism, and glutamate metabolism, as well as valine/leucine/isoleucine metabolism are likely dysregulated in cancer dormancy. These findings provide new insights and molecular pathway targets on cancer dormancy, comprehensively catalog dormancy-associated metabolic pathways, and inform future research aimed at prevention of cancer recurrence in particular.
MeSH term(s)	Humans ; Metabolic Networks and Pathways/genetics ; Neoplasms/genetics ; Transcriptome/genetics
Language	English
Publishing date	2022-04-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2030312-9
ISSN	1557-8100 ; 1536-2310
ISSN (online)	1557-8100
ISSN	1536-2310
DOI	10.1089/omi.2022.0008
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Article ; Online: Autophagy as a Cellular Stress Response Mechanism in the Nervous System.

Peker, Nesibe / Gozuacik, Devrim

Journal of molecular biology

2020 Volume 432, Issue 8, Page(s) 2560–2588

Abstract: Cells of an organism face with various types of insults during their lifetime. Exposure to toxins, metabolic problems, ischaemia/reperfusion, physical trauma, genetic diseases, neurodegenerative diseases are among the conditions that trigger cellular ... ...

Abstract	Cells of an organism face with various types of insults during their lifetime. Exposure to toxins, metabolic problems, ischaemia/reperfusion, physical trauma, genetic diseases, neurodegenerative diseases are among the conditions that trigger cellular stress responses. In this context, autophagy is one of the mechanisms that supports cell survival under stressful conditions. Autophagic vesicle engulfs the cargo and transports it to lysosome for degradation and turnover. As such, autophagy eliminates abnormal proteins, clears damaged organelles, limits oxidative stress and helps to improve metabolic balance. Nervous system cells and particularly postmitotic neurons are highly sensitive to a spectrum of insults, and autophagy emerges as one of the key stress response mechanism, ensuring health and survival of these vulnerable cell types. In this review, we will overview mechanisms through which cells cope with stress, and how these stress responses regulate autophagy, with a special focus on the nervous system.
MeSH term(s)	Animals ; Autophagy ; Homeostasis ; Humans ; Neurodegenerative Diseases/pathology ; Oxidative Stress
Language	English
Publishing date	2020-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2020.01.017
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Zs.A 867: Show issues

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Article ; Online: MicroRNAs as major regulators of the autophagy pathway.

Akkoc, Yunus / Gozuacik, Devrim

Biochimica et biophysica acta. Molecular cell research

2020 Volume 1867, Issue 5, Page(s) 118662

Abstract: Autophagy is a cellular stress response mechanism activation of which leads to degradation of cellular components, including proteins as well as damaged organelles in lysosomes. Defects in autophagy mechanisms were associated with several pathologies (e ... ...

Abstract	Autophagy is a cellular stress response mechanism activation of which leads to degradation of cellular components, including proteins as well as damaged organelles in lysosomes. Defects in autophagy mechanisms were associated with several pathologies (e.g. cancer, neurodegenerative diseases, and rare genetic diseases). Therefore, autophagy regulation is under strict control. Transcriptional and post-translational mechanisms that control autophagy in cells and organisms studied in detail. Recent studies introduced non-coding small RNAs, and especially microRNAs (miRNAs) in the post-translational orchestration of the autophagic activity. In this review article, we analyzed in detail the current status of autophagy-miRNA connections. Comprehensive documentation of miRNAs that were directly involved in autophagy regulation resulted in the emergence of common themes and concepts governing these complex and intricate interactions. Hence, a better and systematic understanding of these interactions reveals a central role for miRNAs in the regulation of autophagy.
MeSH term(s)	Autophagy ; Gene Expression Regulation ; Gene Regulatory Networks ; Genetic Predisposition to Disease ; Humans ; MicroRNAs/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2020-01-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2020.118662
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Uc I Zs.247: Show issues

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Article ; Online: Autophagy and liver cancer.

Akkoç, Yunus / Gözüaçık, Devrim

The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology

2018 Volume 29, Issue 3, Page(s) 270–282

Abstract: Autophagy is a key biological phenomenon conserved from yeast to mammals. Under basal conditions, activation of autophagy leads to the protein degradation as well as damaged organelles for maintaining cellular homeostasis. Deregulation of autophagy has ... ...

Abstract	Autophagy is a key biological phenomenon conserved from yeast to mammals. Under basal conditions, activation of autophagy leads to the protein degradation as well as damaged organelles for maintaining cellular homeostasis. Deregulation of autophagy has been identified as a key mechanism contributing to the pathogenesis and progression of several liver diseases, including hepatocellular carcinoma (HCC), one of the most common and mortal types of cancer. Currently used treatment strategies in patients with HCC result in variable success rates. Therefore, novel early diagnosis and treatment techniques should be developed. Manipulation of autophagy may improve responses of cancer cell to treatments and provide novel targeted therapy options for HCC. In this review, we summarized how our understanding of autophagy-cell death connection may have an impact on HCC therapy.
MeSH term(s)	Autophagy/physiology ; Carcinoma, Hepatocellular/physiopathology ; Hepatocytes/physiology ; Humans ; Liver/cytology ; Liver/physiopathology ; Liver Neoplasms/physiopathology
Language	English
Publishing date	2018-05-10
Publishing country	Turkey
Document type	Journal Article ; Review
ZDB-ID	1340275-4
ISSN	2148-5607 ; 1300-4948
ISSN (online)	2148-5607
ISSN	1300-4948
DOI	10.5152/tjg.2018.150318
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Zs.A 4524: Show issues

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Article ; Online: Crosstalk between autophagy and DNA repair systems.

Demirbağ-Sarikaya, Sinem / Çakir, Hatice / Gözüaçik, Devrim / Akkoç, Yunus

Turkish journal of biology = Turk biyoloji dergisi

2021 Volume 45, Issue 3, Page(s) 235–252

Abstract: Autophagy and DNA repair are two essential biological mechanisms that maintain cellular homeostasis. Impairment of these mechanisms was associated with several pathologies such as premature aging, neurodegenerative diseases, and cancer. Intrinsic or ... ...

Abstract	Autophagy and DNA repair are two essential biological mechanisms that maintain cellular homeostasis. Impairment of these mechanisms was associated with several pathologies such as premature aging, neurodegenerative diseases, and cancer. Intrinsic or extrinsic stress stimuli (e.g., reactive oxygen species or ionizing radiation) cause DNA damage. As a biological stress response, autophagy is activated following insults that threaten DNA integrity. Hence, in collaboration with DNA damage repair and response mechanisms, autophagy contributes to the maintenance of genomic stability and integrity. Yet, connections and interactions between these two systems are not fully understood. In this review article, current status of the associations and crosstalk between autophagy and DNA repair systems is documented and discussed.
Language	English
Publishing date	2021-06-23
Publishing country	Turkey
Document type	Journal Article
ZDB-ID	2046470-8
ISSN	1303-6092 ; 1300-0152
ISSN (online)	1303-6092
ISSN	1300-0152
DOI	10.3906/biy-2103-51
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Article: Autophagy and Cancer Dormancy.

Akkoc, Yunus / Peker, Nesibe / Akcay, Arzu / Gozuacik, Devrim

Frontiers in oncology

2021 Volume 11, Page(s) 627023

Abstract: Metastasis and relapse account for the great majority of cancer-related deaths. Most metastatic lesions are micro metastases that have the capacity to remain in a non-dividing state called "dormancy" for months or even years. Commonly used anticancer ... ...

Abstract	Metastasis and relapse account for the great majority of cancer-related deaths. Most metastatic lesions are micro metastases that have the capacity to remain in a non-dividing state called "dormancy" for months or even years. Commonly used anticancer drugs generally target actively dividing cancer cells. Therefore, cancer cells that remain in a dormant state evade conventional therapies and contribute to cancer recurrence. Cellular and molecular mechanisms of cancer dormancy are not fully understood. Recent studies indicate that a major cellular stress response mechanism, autophagy, plays an important role in the adaptation, survival and reactivation of dormant cells. In this review article, we will summarize accumulating knowledge about cellular and molecular mechanisms of cancer dormancy, and discuss the role and importance of autophagy in this context.
Language	English
Publishing date	2021-03-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2021.627023
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Article: Glutamate Scavenging as a Neuroreparative Strategy in Ischemic Stroke.

Kaplan-Arabaci, Oykum / Acari, Alperen / Ciftci, Pinar / Gozuacik, Devrim

Frontiers in pharmacology

2022 Volume 13, Page(s) 866738

Abstract: Stroke is the second highest reason of death in the world and the leading cause of disability. The ischemic stroke makes up the majority of stroke cases that occur due to the blockage of blood vessels. Therapeutic applications for ischemic stroke include ...

Abstract	Stroke is the second highest reason of death in the world and the leading cause of disability. The ischemic stroke makes up the majority of stroke cases that occur due to the blockage of blood vessels. Therapeutic applications for ischemic stroke include thrombolytic treatments that are in limited usage and only applicable to less than 10% of the total stroke patients, but there are promising new approaches. The main cause of ischemic neuronal death is glutamate excitotoxicity. There have been multiple studies focusing on neuroprotection via reduction of glutamate both in ischemic stroke and other neurodegenerative diseases that ultimately failed due to the obstacles in delivery. At that point, systemic glutamate grabbing, or scavenging is an ingenious way of decreasing glutamate levels upon ischemic stroke. The main advantage of this new therapeutic method is the scavengers working in the circulating blood so that there is no interference with the natural brain neurophysiology. In this review, we explain the molecular mechanisms of ischemic stroke, provide brief information about existing drugs and approaches, and present novel systemic glutamate scavenging methods. This review hopefully will elucidate the potential usage of the introduced therapeutic approaches in stroke patients.
Language	English
Publishing date	2022-03-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.866738
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