ESCRT-III-mediated membrane repair in cell death and tumor resistance

Liu, Jiao; Kang, Rui; Tang, Daolin

doi:10.1038/s41417-020-0200-0

Cited by 80 publications

(52 citation statements)

References 36 publications

(40 reference statements)

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“…However, the process and function of ferroptosis needs to be explored. An unresolved central issue is that these oxidative damage, antioxidant defense mechanisms, and membrane repair mechanisms are also involved in the regulation of other kinds of non-ferroptotic cell death (Bae et al, 2011;Liu et al, 2020a). Thus, although they may share a common upstream mechanism, the identification of unique downstream effectors may distinguish ferroptosis from non-ferroptotic cell death.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Damage and Antioxidant Defense in Ferroptosis

Kuang

Liu

Tang

et al. 2020

Front. Cell Dev. Biol.

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354

197

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Many new types of regulated cell death have been recently implicated in human health and disease. These regulated cell deaths have different morphological, genetic, biochemical, and functional hallmarks. Ferroptosis was originally described as a carcinogenic RAS-dependent non-apoptotic cell death, and is now defined as a type of regulated necrosis characterized by iron accumulation, lipid peroxidation, and the release of damage-associated molecular patterns (DAMPs). Multiple oxidative and antioxidant systems, acting together autophagy machinery, shape the process of lipid peroxidation during ferroptosis. In particular, the production of reactive oxygen species (ROS) that depends on the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and the mitochondrial respiratory chain promotes lipid peroxidation by lipoxygenase (ALOX) or cytochrome P450 reductase (POR). In contrast, the glutathione (GSH), coenzyme Q10 (CoQ10), and tetrahydrobiopterin (BH 4) system limits oxidative damage during ferroptosis. These antioxidant processes are further transcriptionally regulated by nuclear factor, erythroid 2-like 2 (NFE2L2/NRF2), whereas membrane repair during ferroptotic damage requires the activation of endosomal sorting complexes required for transport (ESCRT)-III. A further understanding of the process and function of ferroptosis may provide precise treatment strategies for disease.

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Section: Discussionmentioning

confidence: 99%

Oxidative Damage and Antioxidant Defense in Ferroptosis

Kuang

Liu

Tang

et al. 2020

Front. Cell Dev. Biol.

Self Cite

354

197

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“…Various miRs have been identified as attractive therapeutic markers for neurocognitive disorders [ 140 ], cancer [ 141 ], metabolic syndrome [ 142 ], and autoimmune diseases [ 143 , 144 ]. miRs-based therapies are classified as miRs mimics and anti-miRs oligonucleotides.…”

Section: Mirs-based Therapeuticsmentioning

confidence: 99%

Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity

Kiran

Kumar

et al. 2021

Cells

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Obesity is characterized as a complex and multifactorial excess accretion of adipose tissue (AT) accompanied with alterations in the immune response that affects virtually all age and socioeconomic groups around the globe. The abnormal accumulation of AT leads to several metabolic diseases, including nonalcoholic fatty liver disorder (NAFLD), low-grade inflammation, type 2 diabetes mellitus (T2DM), cardiovascular disorders (CVDs), and cancer. AT is an endocrine organ composed of adipocytes and immune cells, including B-Cells, T-cells and macrophages. These immune cells secrete various cytokines and chemokines and crosstalk with adipokines to maintain metabolic homeostasis and low-grade chronic inflammation. A novel form of adipokines, microRNA (miRs), is expressed in many developing peripheral tissues, including ATs, T-cells, and macrophages, and modulates the immune response. miRs are essential for insulin resistance, maintaining the tumor microenvironment, and obesity-associated inflammation (OAI). The abnormal regulation of AT, T-cells, and macrophage miRs may change the function of different organs including the pancreas, heart, liver, and skeletal muscle. Since obesity and inflammation are closely associated, the dysregulated expression of miRs in inflammatory adipocytes, T-cells, and macrophages suggest the importance of miRs in OAI. Therefore, in this review article, we have elaborated the role of miRs as epigenetic regulators affecting adipocyte differentiation, immune response, AT browning, adipogenesis, lipid metabolism, insulin resistance (IR), glucose homeostasis, obesity, and metabolic disorders. Further, we will discuss a set of altered miRs as novel biomarkers for metabolic disease progression and therapeutic targets for obesity.

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“…Although, there are no publication regarding the importance of CHMP7 gene in HCC, activation of ESCRT-III machinery leads to membrane repair by shedding damaged parts of cell membranes. ESCRT-III is associated with resistance to cell death, especially when treated with anticancer agents [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

The pattern of gene copy number alteration (CNAs) in hepatocellular carcinoma: an in silico analysis

et al. 2021

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Background Hepatocellular carcinoma (HCC) is the most common type of liver cancer that occurs predominantly in patients with previous liver conditions. In the absence of an ideal screening modality, HCC is usually diagnosed at an advanced stage. Recent studies show that loss or gain of genomic materials can activate the oncogenes or inactivate the tumor suppressor genes to predispose cells toward carcinogenesis. Here, we evaluated both the copy number alteration (CNA) and RNA sequencing data of 361 HCC samples in order to locate the frequently altered chromosomal regions and identify the affected genes. Results Our data show that the chr1q and chr8p are two hotspot regions for genomic amplifications and deletions respectively. Among the amplified genes, YY1AP1 (chr1q22) possessed the largest correlation between CNA and gene expression. Moreover, it showed a positive correlation between CNA and tumor grade. Regarding deleted genes, CHMP7 (chr8p21.3) possessed the largest correlation between CNA and gene expression. Protein products of both genes interact with other cellular proteins to carry out various functional roles. These include ASH1L, ZNF496, YY1, ZMYM4, CHMP4A, CHMP5, CHMP2A and CHMP3, some of which are well-known cancer-related genes. Conclusions Our in-silico analysis demonstrates the importance of copy number alterations in the pathology of HCC. These findings open a door for future studies that evaluate our results by performing additional experiments.

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ESCRT-III-mediated membrane repair in cell death and tumor resistance

Cited by 80 publications

References 36 publications

Oxidative Damage and Antioxidant Defense in Ferroptosis

Oxidative Damage and Antioxidant Defense in Ferroptosis

Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity

The pattern of gene copy number alteration (CNAs) in hepatocellular carcinoma: an in silico analysis

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