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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: 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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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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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 ; 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 ; Online: Artificial intelligence assisted patient blood and urine droplet pattern analysis for non-invasive and accurate diagnosis of bladder cancer.

Demir, Ramiz / Koc, Soner / Ozturk, Deniz Gulfem / Bilir, Sukriye / Ozata, Halil İbrahim / Williams, Rhodri / Christy, John / Akkoc, Yunus / Tinay, İlker / Gunduz-Demir, Cigdem / Gozuacik, Devrim

Scientific reports

2024 Volume 14, Issue 1, Page(s) 2488

Abstract: Bladder cancer is one of the most common cancer types in the urinary system. Yet, current bladder cancer diagnosis and follow-up techniques are time-consuming, expensive, and invasive. In the clinical practice, the gold standard for diagnosis remains ... ...

Abstract	Bladder cancer is one of the most common cancer types in the urinary system. Yet, current bladder cancer diagnosis and follow-up techniques are time-consuming, expensive, and invasive. In the clinical practice, the gold standard for diagnosis remains invasive biopsy followed by histopathological analysis. In recent years, costly diagnostic tests involving the use of bladder cancer biomarkers have been developed, however these tests have high false-positive and false-negative rates limiting their reliability. Hence, there is an urgent need for the development of cost-effective, and non-invasive novel diagnosis methods. To address this gap, here we propose a quick, cheap, and reliable diagnostic method. Our approach relies on an artificial intelligence (AI) model to analyze droplet patterns of blood and urine samples obtained from patients and comparing them to cancer-free control subjects. The AI-assisted model in this study uses a deep neural network, a ResNet network, pre-trained on ImageNet datasets. Recognition and classification of complex patterns formed by dried urine or blood droplets under different conditions resulted in cancer diagnosis with a high specificity and sensitivity. Our approach can be systematically applied across droplets, enabling comparisons to reveal shared spatial behaviors and underlying morphological patterns. Our results support the fact that AI-based models have a great potential for non-invasive and accurate diagnosis of malignancies, including bladder cancer.
MeSH term(s)	Humans ; Artificial Intelligence ; Reproducibility of Results ; Urinary Bladder Neoplasms/pathology ; Urinary Bladder/pathology ; Biomarkers, Tumor/urine
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2024-01-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-52728-7
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Article ; Online: Transcriptional landscape of cellular networks reveal interactions driving the dormancy mechanisms in cancer.

Uzuner, Dilara / Akkoç, Yunus / Peker, Nesibe / Pir, Pınar / Gözüaçık, Devrim / Çakır, Tunahan

Scientific reports

2021 Volume 11, Issue 1, Page(s) 15806

Abstract: Primary cancer cells exert unique capacity to disseminate and nestle in distant organs. Once seeded in secondary sites, cancer cells may enter a dormant state, becoming resistant to current treatment approaches, and they remain silent until they ... ...

Abstract	Primary cancer cells exert unique capacity to disseminate and nestle in distant organs. Once seeded in secondary sites, cancer cells may enter a dormant state, becoming resistant to current treatment approaches, and they remain silent until they reactivate and cause overt metastases. To illuminate the complex mechanisms of cancer dormancy, 10 transcriptomic datasets from the literature enabling 21 dormancy-cancer comparisons were mapped on protein-protein interaction networks and gene-regulatory networks to extract subnetworks that are enriched in significantly deregulated genes. The genes appearing in the subnetworks and significantly upregulated in dormancy with respect to proliferative state were scored and filtered across all comparisons, leading to a dormancy-interaction network for the first time in the literature, which includes 139 genes and 1974 interactions. The dormancy interaction network will contribute to the elucidation of cellular mechanisms orchestrating cancer dormancy, paving the way for improvements in the diagnosis and treatment of metastatic cancer.
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Computational Biology/methods ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Humans ; Mice ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Precancerous Conditions/genetics ; Precancerous Conditions/metabolism ; Precancerous Conditions/pathology ; Transcriptome
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2021-08-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-94005-x
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Article ; Online: A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress.

Demirbag-Sarikaya, Sinem / Akkoc, Yunus / Turgut, Sıla / Erbil-Bilir, Secil / Kocaturk, Nur Mehpare / Dengjel, Joern / Gozuacik, Devrim

Scientific reports

2022 Volume 12, Issue 1, Page(s) 8134

Abstract: The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved ... ...

Abstract	The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved stress response pathway that is activated by various insults including DNA damage. All sorts of damage to DNA potentially cause loss of genetic information and trigger genomic instability. Most of these lesions are repaired by the activation of DNA damage response following DNA repair mechanisms. Here we describe, a novel protein complex containing the autophagy protein ATG5 and the non-homologous end-joining repair system proteins. We discovered for the first time that ATG5 interacted with both Ku80 (XRCC5) and Ku70 (XRCC6). This novel interaction is facilitated mainly via Ku70. Our results suggest that this interaction is dynamic and enhanced upon genotoxic stresses. Strikingly, we identified that ATG5-Ku70 interaction is necessary for DNA repair and effective recovery from genotoxic stress. Therefore, our results are demonstrating a novel, direct, dynamic, and functional interaction between ATG5 and Ku70 proteins that plays a crucial role in DNA repair under genotoxic stress conditions.
MeSH term(s)	Antigens, Nuclear/genetics ; Antigens, Nuclear/metabolism ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; DNA Damage ; DNA End-Joining Repair ; DNA Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Genomic Instability ; Humans ; Ku Autoantigen/metabolism
Chemical Substances	ATG5 protein, human ; Antigens, Nuclear ; Autophagy-Related Protein 5 ; DNA-Binding Proteins ; Ku Autoantigen (EC 4.2.99.-)
Language	English
Publishing date	2022-05-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-11704-9
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Article ; Online: Novel protein complexes containing autophagy and UPS components regulate proteasome-dependent PARK2 recruitment onto mitochondria and PARK2-PARK6 activity during mitophagy.

Kocaturk, Nur Mehpare / Peker, Nesibe / Eberhart, Karin / Akkoc, Yunus / Deveci, Gamze / Dengjel, Joern / Gozuacik, Devrim

Cell death & disease

2022 Volume 13, Issue 11, Page(s) 947

Abstract: Autophagy is an evolutionarily conserved eukaryotic cellular mechanism through which cytosolic fragments, misfolded/aggregated proteins and organelles are degraded and recycled. Priming of mitochondria through ubiquitylation is required for the clearance ...

Abstract	Autophagy is an evolutionarily conserved eukaryotic cellular mechanism through which cytosolic fragments, misfolded/aggregated proteins and organelles are degraded and recycled. Priming of mitochondria through ubiquitylation is required for the clearance the organelle by autophagy (mitophagy). Familial Parkinson's Disease-related proteins, including the E3-ligase PARK2 (PARKIN) and the serine/threonine kinase PARK6 (PINK1) control these ubiquitylation reactions and contribute to the regulation of mitophagy. Here we describe, novel protein complexes containing autophagy protein ATG5 and ubiquitin-proteasome system (UPS) components. We discovered that ATG5 interacts with PSMA7 and PARK2 upon mitochondrial stress. Results suggest that all three proteins translocate mitochondria and involve in protein complexes containing autophagy, UPS and mitophagy proteins. Interestingly, PARK2 and ATG5 recruitment onto mitochondria requires proteasome components PSMA7 and PSMB5. Strikingly, we discovered that subunit of 20 S proteasome, PSMA7, is required for the progression of PARK2-PARK6-mediated mitophagy and the proteasome activity following mitochondrial stress. Our results demonstrate direct, dynamic and functional interactions between autophagy and UPS components that contribute to the regulation of mitophagy.
MeSH term(s)	Humans ; Mitophagy/physiology ; Ubiquitin/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Parkinson Disease/metabolism ; Mitochondria/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Autophagy/physiology
Chemical Substances	Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-11-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-022-05339-x
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