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Introduction The word ‘autophagy’ derives from the Greek roots ‘auto,’ or self, and ‘phagy,’ to eat ( Levine & Klionsky 2004 ) – in other words, self-cannibalism or self-eating. Autophagy is a genetically programmed and evolutionarily conserved
Shanghai Jiao Tong University School of Medicine, Shanghai, China
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kinase. A full color version of this figure is available at https://doi.org/10.1530/ERC-18-0502 . Macroautophagy (hereafter referred to as autophagy) is a process that captures and degrades intracellular components in lysosomes, thereby
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search for novel molecular targeted drugs for the cure of such highly malignant thyroid cancers. Figure 1 Autophagy-targeted opportunities for the therapy of thyroid cancers. Origin and aggressive phenotypes of thyroid cancers and opportunities for
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FAM129A acts is not completely understood. Considering that autophagy is rapidly upregulated under cell stress, such as nutrient starvation, growth factor depletion, reactive oxygen species (ROS) accumulation and ER stress ( Kroemer et al. 2010
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Department of Surgery, Wake Forest University, Winston-Salem, North Carolina, USA
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Faculty of Pharmaceutical Sciences, Department of Food and Experimental Nutrition, University of São Paulo, São Paulo, Brazil
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al . 2013 ). Initially, the UPR functions as an adaptive response to maintain normal physiological functions and to protect the cells from irreversible damage. UPR further induces autophagy that can either eliminate cancer cells ( Fulda et al . 2010
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. 2012 , De Picciotto et al. 2016 ). Furthermore, mechanisms of BRCA2 impacting on the responses to platinum have not been thoroughly elucidated. Autophagy is commonly considered a survival pathway, but can be cytotoxic when the damage is critical
Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, People’s Republic of China
Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
Clinical Research Center for Cancer of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
Clinical Research Center for Cancer of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
Clinical Research Center for Cancer of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, People’s Republic of China
Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Otolaryngology & Head and Neck Center, Cancer Center, Department of Head and Neck Surgery, Zhejiang Provincial People’s Hospital (Affiliated People’s Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, People’s Republic of China
Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
Clinical Research Center for Cancer of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
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Key Laboratory of Endocrine Gland Diseases of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
Clinical Research Center for Cancer of Zhejiang Province, Hangzhou, Zhejiang, People’s Republic of China
Department of Thyroid and Breast Surgery, Zhejiang Provincial People’s Hospital Bijie Hospital, Bijie, Guizhou, China
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.05; ** P < 0.01. Autophagic blockade potentiated anlotinib-mediated ferroptosis Accumulating studies have shown that autophagy functions importantly during ferroptosis ( Dai et al. 2020 , Wei et al. 2020 ). Therefore, autophagic
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, Avniel-Polak et al . 2015 ). However, it has been shown that mTORC1 prevents the generation of autophagosomes and the initiation of autophagy through phosphorylation of ULK1; the administration of mTORi such as RAD001 inhibits mTORC1, preventing
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required. Autophagy is a lysosomal degenerative pathway of organelles or foreign proteins that supplies amino acids to meet the metabolic demands of cells ( Klionsky & Emr 2000 ). Thus, the inhibition of autophagy is a potential target for treating
Cancer Genetics, Department of Endocrinology, Kolling Institute of Medical Research
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Cancer Genetics, Department of Endocrinology, Kolling Institute of Medical Research
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Cancer Genetics, Department of Endocrinology, Kolling Institute of Medical Research
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Introduction Autophagy is a eukaryotic cell process of self-catabolic degradation originally described in the 1960's ( Deter & De Duve 1967 ). The term autophagy is derived from Greek terminology ‘auto’ (meaning self) and ‘phagy’ (eating) to