Erratum: Cystatin SN inhibits auranofin-induced cell death by autophagic induction and ROS regulation via glutathione reductase activity in colorectal cancer

Oh, Byung Moo; Lee, Seon-Jin; Cho, Hee Jun; Park, Yun Sun; Kim, Jong-Tae; Yoon, Suk Ran; Lee, Sang Chul; Lim, Jong‐Seok; Kim, Bo-Yeon; Choe, Yong-Kyung; Lee, Hee Gu

doi:10.1038/cddis.2017.446

Cited by 9 publications

(4 citation statements)

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“…Cell death induced by 2c and similar compounds is characterized by: (i) the accumulation of poly-ubiquitylated proteins, (ii) the induction of oxidative stress response and (iii) of the unfolded protein response (UPR) 1 , 8 , 14 , 17 . To verify that the presence of the biotin tag does not influence the activation of these cellular responses, we initially investigated the accumulation of polyubiquitylated proteins.…”

Section: Resultsmentioning

confidence: 99%

The binding landscape of a partially-selective isopeptidase inhibitor with potent pro-death activity, based on the bis(arylidene)cyclohexanone scaffold

et al. 2018

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Diaryldienone derivatives with accessible β-carbons show strong anti-neoplastic properties, related to their ability to make covalent adducts with free thiols by Michael addition, and low toxicity in vivo. Accumulation of poly-ubiquitylated proteins, activation of the unfolded protein response (UPR) and induction of cell death are universal hallmarks of their activities. These compounds have been characterized as inhibitors of isopeptidases, a family of cysteine-proteases, which de-conjugate ubiquitin and ubiquitin-like proteins from their targets. However, it is unclear whether they can also react with additional proteins. In this work, we utilized the biotin-conjugated diaryldienone-derivative named 2c, as a bait to purify novel cellular targets of these small molecules. Proteomic analyses have unveiled that, in addition to isopeptidases, these inhibitors can form stable covalent adducts with different intracellular proteins, thus potentially impacting on multiple functions of the cells, from cytoskeletal organization to metabolism. These widespread activities can explain the ability of diaryldienone derivatives to efficiently trigger different cell death pathways.

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Section: Resultsmentioning

confidence: 99%

The binding landscape of a partially-selective isopeptidase inhibitor with potent pro-death activity, based on the bis(arylidene)cyclohexanone scaffold

et al. 2018

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“…The presence of DNA damage activates a robust response named the DNA damage response (DDR) (Calcinotto et al, 2019). Common DDR outcomes realized from intrinsic insults include telomere shortening (Azarm et al, 2020), oncogene mutation (Hafez et al, 2017), and oxidative damage (Oh et al, 2017). Various DNA-damaging agents are also effectively applied to induce different types of senescence, for example, chemotherapy-induced senescence (e.g., that induced by doxorubicin (Yao et al, 2020) or etoposide (Zurgil et al, 2014)).…”

Section:  Extracellular Vesicles In the Cellular Senescence And Aging Microenvironment  Cellular Senescence And The Aging Microenvironmentioning

confidence: 99%

Roles of extracellular vesicles in the aging microenvironment and age‐related diseases

Yin

Chen

Wang

et al. 2021

J of Extracellular Vesicle

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Cellular senescence is a persistently hypoproliferative state with diverse stressors in a specific aging microenvironment. Senescent cells have a double-edged sword effect: they can be physiologically beneficial for tissue repair, organ growth, and body homeostasis, and they can be pathologically harmful in age-related diseases. Among the hallmarks of senescence, the SASP, especially SASP-related extracellular vesicle (EV) signalling, plays the leading role in aging transmission via paracrine and endocrine mechanisms. EVs are successful in intercellular and interorgan communication in the aging microenvironment and age-related diseases. They have detrimental effects on downstream targets at the levels of immunity, inflammation, gene expression, and metabolism. Furthermore, EVs obtained from different donors are also promising materials and tools for antiaging treatments and are used for regeneration and rejuvenation in cell-free systems. Here, we describe the characteristics of cellular senescence and the aging microenvironment, concentrating on the production and function of EVs in age-related diseases, and provide new ideas for antiaging therapy with EVs.

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“…This previously unobserved phenomenon demonstrates that the success of therapeutic candidates for "block and lock" or "shock and kill" could be hampered by the cellular diversity of the latent reservoir. Auranofin, an FDA-approved compound commonly used for the treatment of rheumatoid arthritis, was previously investigated in clinical trials for potential therapeutic applications in diseases such as cancer (72)(73)(74) and HIV (25,75). It was previously shown to decrease the cell-associated viral DNA reservoir in peripheral blood of macaques infected with SIVmac251 (HIV-1 homologue simian immunodeficiency virus) when used in combination with ART (26).…”

Section: Discussionmentioning

confidence: 99%

Monocyte to macrophage differentiation and changes in cellular redox homeostasis promote cell type-specific HIV latency reactivation

Blanco,

Coronado,

Arun

et al. 2024

Preprint

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Human Immunodeficiency Virus (HIV) latency regulation in monocytes and macrophages can vary according to signals directing differentiation, polarization, and function. To investigate these processes, we generated an HIV latency model in THP-1 monocytes and showed differential levels of HIV reactivation among clonal populations. Monocyte-to-macrophage differentiation of HIV-infected primary human CD14+ and THP-1 cells induced HIV reactivation and showed that virus production increased concomitant with macrophage differentiation. We applied the HIV-infected THP-1 monocyte-to-macrophage (MLat) model to assess the biological mechanisms regulating HIV latency dynamics during monocyte-to-macrophage differentiation. We pinpointed PKC signaling pathway activation and Cyclin T1 upregulation as inherent differentiation mechanisms that regulate HIV latency reactivation. Macrophage polarization regulated latency, revealing pro-inflammatory M1 macrophages suppressed HIV reactivation while M2 macrophages promoted HIV reactivation. Because macrophages rely on reactive-oxygen species (ROS) to exert numerous cellular functions, we disrupted redox pathways and discovered that inhibitors of the thioredoxin (Trx) system acted as latency promoting agents (LPAs) in T-cells and monocytes, but opposingly acted as latency reversing agents (LRAs) in macrophages. We explored this mechanism with Auranofin, a clinical candidate for reducing HIV reservoirs, and demonstrated Trx reductase (TrxR) inhibition led to ROS induced NF-κB activity, which promoted HIV reactivation in macrophages, but not in T-cells and monocytes. Collectively, cell type-specific differences in HIV latency regulation could pose a barrier to HIV eradication strategies.

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Erratum: Cystatin SN inhibits auranofin-induced cell death by autophagic induction and ROS regulation via glutathione reductase activity in colorectal cancer

Cited by 9 publications

References 0 publications

The binding landscape of a partially-selective isopeptidase inhibitor with potent pro-death activity, based on the bis(arylidene)cyclohexanone scaffold

The binding landscape of a partially-selective isopeptidase inhibitor with potent pro-death activity, based on the bis(arylidene)cyclohexanone scaffold

Roles of extracellular vesicles in the aging microenvironment and age‐related diseases

Monocyte to macrophage differentiation and changes in cellular redox homeostasis promote cell type-specific HIV latency reactivation

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