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autophagic cell death induced by reactive oxygen species is involved in hyperthermic sensitization to ionizing radiation in human hepatocellular carcinoma cells

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World Journal of Gastroenterology 2017年第30期23卷 5530-5537页

作者： Guang-Jin Yuan Jun-Jian Deng De-Dong Cao Lei Shi Xin Chen Jin-Ju Lei Xi-Ming Xu Department of Oncology Nationality Hospital of Qianjiang Cancer Center Renmin Hospital of Wuhan University

AIM To investigate whether autophagic cell death is involved in hyperthermic sensitization to ionizing radiation in human hepatocellular carcinoma cells, and to explore the underlying *** Human hepatocellular carcinoma cells were treated with hyperthermia and ionizing radiation. MTT and clonogenic assays were performed to determine cell survival. cell autophagy was detected using acridine orange staining and flow cytometric analysis, and the expression of autophagy-associated proteins, LC3 and p62, was determined by Western blot analysis. Intracellular reactive oxygen species(ROS) were quantified using the fluorescent probe *** Treatment with hyperthermia and ionizing radiation significantly decreased cell viability and surviving fraction as compared with hyperthermia or ionizing radiation alone. cell autophagy was significantly increased after ionizing radiation combined with hyperthermia treatment, as evidenced by increased formation of acidic vesicular organelles, increased expression of LC3 II and decreased expression of p62. Intracellular ROS were also increased after combined treatment with hyperthermia and ionizing radiation. Pretreatment with N-acetylcysteine, an ROS scavenger, markedly inhibited the cytotoxicity and cell autophagy induced by hyperthermia and ionizing *** autophagic cell death is involved in hyperthermic sensitization of cancer cells to ionizing radiation, and its induction may be due to the increased intracellular ROS.

关键词： autophagic cell death Hyperthermia Ionizing radiation Hepatocellular carcinoma Reactive oxygen species

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Autophagy prevents autophagic cell death in Tetrahymena in response to oxidative stress

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Zoological Research 2015年第3期36卷 167-173页

作者： Si-Wei ZHANG Jiang-Nan FENG Yi CAO Li-Ping MENG Shu-Lin WANG State Key Laboratory of Genetic Engineering Institute of GeneticsSchool of Life SciencesFudan University

Autophagy is a major cellular pathway used to degrade long-lived proteins or organelles that may be damaged due to increased reactive oxygen species（ROS） generated by cellular stress. Autophagy typically enhances cell survival, but it may also act to promote cell death under certain conditions. The mechanism underlying this paradox, however, remains unclear. We showed that Tetrahymena cells exerted increased membranebound vacuoles characteristic of autophagy followed by autophagic cell death（referred to as cell death with autophagy） after exposure to hydrogen peroxide. Inhibition of autophagy by chloroquine or 3-methyladenine significantly augmented autophagic cell death induced by hydrogen peroxide. Blockage of the mitochondrial electron transport chain or starvation triggered activation of autophagy followed by cell death by inducing the production of ROS due to the loss of mitochondrial membrane potential. This indicated a regulatory role of mitochondrial ROS in programming autophagy and autophagic cell death in Tetrahymena. Importantly, suppression of autophagy enhanced autophagic cell death in Tetrahymena in response to elevated ROS production from starvation, and this was reversed by antioxidants. Therefore, our results suggest that autophagy was activated upon oxidative stress to prevent the initiation of autophagic cell death in Tetrahymena until the accumulation of ROS passed the point of no return, leading to delayed cell death in Tetrahymena.

关键词： Autophagy autophagic cell death Lysosome Mitochondria Reactive oxygen species Tetrahymena

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Aβ1-42 induces ROS-mediated autophagic cell death in U87 and SHSY5Y cells

Aβ1-42 induces ROS-mediated autophagic cell death in U87 an...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Hong-Mei WANG~(1,2),Jian-Fang MA~1,Yu-Yan TAN~(1,2),Zhi-Quan WANG~1,Cheng-Yu SHENG~1,Jian-Qing DING~(1,2),Sheng-Di CHEN~(1,2,*) 1 Department of Neurology & Institute of Neurology,Ruijin Hospital,Shanghai Jiaotong University School of Medicine, Shanghai 200025,China 2 Lab of Neurodegenerative Diseases,Institute of Health Science,Shanghai Institutes for Biological Sciences(SIBS), Chinese Academy of Sciences(CAS) & Shanghai Jiaotong University School of Medicine,Shanghai 200025,China

＜正＞Objective Alzheimer’s disease（AD） is a neurodegenerative disorder initiated by the aggregation of amyloidβ-peptide （Aβ）.Macroautophagy,which is essential for cell survival as well as the promotion of cell death,has been observed extensively in AD brains or transgenic mice overexpressing amyloid precursor *** role of macroautophagy in the pathogenesis of AD is,however,*** Acridine orange,transmission electron microscopy and western blotting were performed to detect *** In this study,we showed that Aβ1-42 induced both apoptosis and autophagy in SH-SY5Y cells,whereas it induced only autophagy in U87 cells.Aβ-induced cytotoxicity and autophagic cell death were blocked by the autophagy inhibitor 3-methyladenine（3-MA）.Moreover,following Aβ1-42 treatment,reactive oxygen species（ROS） accumulation was detected.Aβ1-42-induced ROS accumulation was not affected by the addition of ***,treatment with the ROS scavenger N-acetylcysteine inhibited ROS accumulation and autophagic cell death induced by Aβ1-42,suggesting that ROS accumulation might trigger the onset of autophagy and subsequent autophagic cell death in Ap-treated U87 and SH-SY5Y *** addition,siRNA-mediated knockdown of Beclin-1 expression in these cell lines decreased Aβ-induced autophagy and autophagic cell *** SH-S Y5 Y cells, Beclin-1 siRNA had no effect on apoptosis induced by Aβ.Conclusion Collectively,these results suggest that Aβinduces autophagic cell death through a ROS-mediated mechanism.

关键词： autophagic cell death apoptosis Beclin-1 ROS amyloid-βpeptide

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autophagic activity in neuronal cell death

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Neuroscience Bulletin 2015年第4期31卷 382-394页

作者： Robert W.Button Shouqing Luo David C.Rubinsztein Peninsula Schools of Medicine and Dentistry Institute of Translational and Stratified MedicineUniversity of Plymouth Department of Medical Genetics Cambridge Institute for Medical ResearchUniversity of Cambridge

As post-mitotic cells with great energy demands, neurons depend upon the homeostatic and waste-recycling functions provided by autophagy. In addition, autophagy also promotes survival during periods of harsh stress and targets aggregate-prone proteins associated with neurodegeneration for degradation. Despite this, autophagy has also been controversially described as a mechanism of programmed cell death. Instances of autophagic cell death are typically associated with elevated numbers of cytoplasmic autophagosomes, which have been assumed to lead to excessive degradation of cellular components. Due to the high activity and reliance on autophagy in neurons, these cells may be particularly susceptible to autophagic death. In this review, we summarize and assess current evidence in support of autophagic cell death in neurons, as well as how the dysregulation of autophagy commonly seen in neurodegeneration can contribute to neuron loss. From here, we discuss potential treatment strategies relevant to such cell-death pathways.

关键词： autophagy autophagic cell death programmed cell death apoptosis necrosis autosis neurodegeneration

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Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy

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Acta Pharmaceutica Sinica B 2022年第1期12卷 1-17页

作者： Jinjing Wei Yongting Zhao Haihai Liang Weijie Du Lihong Wang Department of Endocrinology the First Affiliated Hospital of Jinan UniversityGuangzhou 510630China Department of Endocrinology the Second Affiliated Hospital of Harbin Medical UniversityHarbin 150081China Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China

Diabetic mellitus(DM) is a common degenerative chronic metabolic disease often accompanied by severe cardiovascular complications(DCCs) as major causes of death in diabetic patients with diabetic cardiomyopathy(DCM) as the most common DCC. The metabolic disturbance in DCM generates the conditions/substrates and inducers/triggers and activates the signaling molecules and death executioners leading to cardiomyocyte death which accelerates the development of DCM and the degeneration of DCM to heart *** forms of programmed active cell death including apoptosis, pyroptosis, autophagic cell death, autosis,necroptosis, ferroptosis and entosis have been identified and characterized in many types of cardiac *** has also been obtained for the presence of multiple forms of cell death in DCM. Most importantly,published animal experiments have demonstrated that suppression of cardiomyocyte death of any forms yields tremendous protective effects on DCM. Herein, we provide the most updated data on the subject of cell death in DCM, critical analysis of published results focusing on the pathophysiological roles of cell death, and pertinent perspectives of future studies.

关键词： Diabetes mellitus Diabetic cardiomyopathy cell death Apoptosis autophagic cell death Aautosis Pyroptosis Necroptosis Ferroptosis

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Suberoylanilide hydroxamic acid upregulates reticulophagy receptor expression and promotes cell death in hepatocellular carcinoma cells

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World Journal of Gastroenterology 2023年第34期29卷 5038-5053页

作者： Jia-Yao Li Tian Tian Bing Han Ting Yang Yi-Xin Guo Jia-Yu Wu Yu-Si Chen Qin Yang Ru-Jia Xie Guizhou Provincial Key Laboratory of Pathogenesis and Drug Research on Common Chronic Diseases College of Basic Medical SciencesGuizhou Medical UniversityGuiyang 550025Guizhou ProvinceChina Department of Pathophysiology College of Basic Medical SciencesGuizhou Medical UniversityGuiyang 550025Guizhou ProvinceChina Department of Eugenic Genetics Guiyang Maternal and Child Health Care HospitalGuiyang 550003Guizhou ProvinceChina

BACKGROUND Hepatocellular carcinoma(HCC)is a common clinical condition with a poor prognosis and few effective treatment *** anticancer agents for treating HCC must be *** plays an essential role in HCC *** hydroxamic acid(SAHA),the most common histone deacetylase inhibitor agent,triggers many forms of cell death in ***,the underlying mechanism of action remains *** with sequence similarity 134 member B(FAM134B)-induced reticulophagy,a selective autophagic pathway,participates in the decision of cell fate and exhibits anticancer *** study focused on the relationship between FAM134B-induced reticulophagy and SAHA-mediated cell *** To elucidate potential roles and underlying molecular mechanisms of reticulophagy in SAHA-induced HCC cell *** The viability,apoptosis,cell cycle,migration,and invasion of SAHA-treated Huh7 and MHCC97L cells were *** related to the reticulophagy pathway,mitochondria-endoplasmic reticulum(ER)contact sites,intrinsic mitochondrial apoptosis,and histone acetylation were quantified using western *** and lysosome colocalization,and mitochondrial Ca^(2+)levels were characterized via confocal *** level of cell death was evaluated through Hoechst 33342 staining and propidium iodide *** immunoprecipitation was used to verify histone H4 lysine-16 acetylation in the FAM134B promoter *** After SAHA treatment,the proliferation of Huh7 and MHCC97L cells was significantly inhibited,and the migration and invasion abilities were greatly blocked in *** promoted apoptosis and caused G1 phase cells to increase in a concentration-dependent *** treatment with SAHA,ER-phagy was activated,thereby triggering autophagy-mediated cell death of HCC cells in *** blotting and chromatin immunoprecipitation assays confirmed that SAHA regulated FAM134B expression by enhancing the hi

关键词： Suberoylanilide hydroxamic acid Histone H4 lysine-16 Reticulophagy Apoptosis autophagic cell death Hepatocellular carcinoma

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