Involvement of Autophagy and Apoptosis in Studies of Anticancer Drugs

Liu, Bo; Ouyang, Liang

doi:10.1016/b978-0-12-405529-2.00018-4

Cited by 2 publications

(1 citation statement)

References 30 publications

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“…UNC51-like kinase 1 is a ubiquitously expressed protein kinase localized to autophagosomal membranes in mammalian cells and shows no special patterns in normal tissues (25). Dominant-negative mutants of ULK1 block autophagy, indicating that ULK1 is an obligatory protein kinase (26). By northern blot analysis, ULK1 mRNA has been detected as multiple bands in heart, brain, spleen, lung, liver and skeletal muscle at varying degrees, indicating that the ubiquitously expressed genes exist in a wide variety of adult tissues, as does its mammalian homologue, ULK2 (6,7).…”

Section: Expression Transcriptional Regulation and Posttranslation Mmentioning

confidence: 99%

UNC51‐like kinase 1, autophagic regulator and cancer therapeutic target

Chen

Tian

et al. 2014

Cell Proliferation

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Autophagy, the cell process of self-digestion, plays a pivotal role in maintaining energy homoeostasis and protein synthesis. When required, it causes degradation of long-lived proteins and damaged organelles, indicating that it may play a dual role in cancer, by both protecting against and promoting cell death. The autophagy-related gene (Atg) family, with more than 35 members, regulates multiple stages of the process. Serine/threonine protein kinase Atg1 in yeast, for example, can interact with other ATG gene products, functioning in autophagosome formation. One mammalian homologue of Atg1, UNC-51-like kinase 1 (ULK1) and its related complex ULK1-mAtg13-FIP200 can mediate autophagy under nutrient-deprived conditions, by protein-protein interactions and post-translational modifications. Although specific mechanisms of how ULK1 and its complex transduces upstream signals to the downstream central autophagy pathways is not fully understood, past studies have indicated that ULK1 can both suppress and promote tumour growth under different conditions. Here, we summarize some properties of ULK1 which can regulate autophagy in cancer, which may shed new light on future cancer therapy strategies, utilizing ULK1 as a potential new target.

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Section: Expression Transcriptional Regulation and Posttranslation Mmentioning

confidence: 99%

UNC51‐like kinase 1, autophagic regulator and cancer therapeutic target

Chen

Tian

et al. 2014

Cell Proliferation

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The Designer Drug 3-Fluoromethcathinone Induces Oxidative Stress and Activates Autophagy in HT22 Neuronal Cells

et al. 2018

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Synthetic cathinones are psychoactive substances, derivatives of a natural psychostimulant cathinone. Although many synthetic cathinones have lost their legal status in many countries, their abuse still continues worldwide. Recently, they have been reported to exert neurotoxic effects in vitro and in vivo. The molecular mechanisms of their action have not been fully elucidated. Recently, they have been linked to the induction of oxidative stress, autophagy, and apoptosis. The aim of this study was to investigate whether 3-fluoromethcathinone (3-FMC), a synthetic cathinone, is able to induce oxidative stress, autophagy, and apoptosis in HT22 immortalized mouse hippocampal cells. We found that treatment of HT22 cells with this compound results in a concentration-dependent increase in the intracellular production of reactive oxygen species. Moreover, 3-FMC induced concentration-dependent conversion of cytosolic LC3-I to membrane-bound LC3-II and formation of autophagic vacuoles. Additionally, the level of p62/SQSTM1 protein decreased after 3-FMC treatment, suggesting that accumulation of autophagic vacuoles resulted from activation rather than inhibition of autophagy. Our results also showed that 3-FMC at millimolar concentration is able to induce caspase-dependent apoptotic cell death in HT22 cells. Our findings suggest that abuse of 3-FMC may disturb neuronal homeostasis and impair functioning of the central nervous system.

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Involvement of Autophagy and Apoptosis in Studies of Anticancer Drugs

Cited by 2 publications

References 30 publications

UNC51‐like kinase 1, autophagic regulator and cancer therapeutic target

UNC51‐like kinase 1, autophagic regulator and cancer therapeutic target

The Designer Drug 3-Fluoromethcathinone Induces Oxidative Stress and Activates Autophagy in HT22 Neuronal Cells

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