Deacetylation of the tumor suppressor protein PML regulates hydrogen peroxide-induced cell death

Guan, Dongyin; Lim, Jun Hee; Peng, Lirong; Liu, Y.; Lam, Minh; Seto, Edward; Kao, Hung‐Ying

doi:10.1038/cddis.2014.185

Cited by 42 publications

(50 citation statements)

References 55 publications

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“…Guan et al. have identified SIRT5 as a deacetylases for the tumor suppressor promyelocytic leukemia protein (PML), suggesting a tumor suppressor function for this SIRT (71). …”

Section: Mitochondrial Sirts and Their Molecular Targets: Relevance Tmentioning

confidence: 99%

Mitochondrial Sirtuins in Cancer: Emerging Roles and Therapeutic Potential

George

Ahmad

2016

Cancer Research

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The past few decades have witnessed a furious attention of scientific community towards identifying novel molecular factors and targets which could be exploited for drug development for cancer management. One such factor is the sirtuin (SIRT) family of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases. The role of SIRTs in cancer is extremely complex, with dichotomous functions depending on cell contexts. Mammalian SIRTs (SIRT1–7), differ in their cellular localization and biological functions. Amongst these, SIRT -3, -4, and -5 are located in the mitochondria and are being carefully investigated. These mitochondrial SIRTs (mtSIRTs) regulate multiple cellular and physiological processes, including cell cycle, gene expression, cell viability, stress response, metabolism and energy homeostasis. Recent research suggests that mtSIRTs influence tumors by regulating the metabolic state of the cell. While the research on the role of mtSIRTs in cancer is still in its infancy, studies have suggested tumor suppressor as well as tumor promoter roles for them. This review is focused on discussing an up-to-date information about the roles and functional relevance of mtSIRTs (SIRT -3, -4, -5) in cancers. We have also provided a critical discussion and our perspective on their dual roles, as tumor promoter versus tumor suppressor, in cancer.

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“…Guan et al. have identified SIRT5 as a deacetylases for the tumor suppressor promyelocytic leukemia protein (PML), suggesting a tumor suppressor function for this SIRT (71). …”

Section: Mitochondrial Sirts and Their Molecular Targets: Relevance Tmentioning

confidence: 99%

Mitochondrial Sirtuins in Cancer: Emerging Roles and Therapeutic Potential

George

Ahmad

2016

Cancer Research

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“…The role of SIRT1 in cell death and survival depends on the type of DNA damage sustained. For example, SIRT1 is required for H 2 O 2 -induced cell death (15,37,38 (Fig. 3, C and D).…”

Section: Sirt1 Ubiquitination Affects Ddr-induced Cell Death and Survmentioning

confidence: 99%

“…SIRT1 is believed to inhibit apoptosis induced by certain types of DNA damage, including IR-and etoposide-induced doublestrand breaks. However, our previous study suggests that SIRT1 promotes cell death in response to stimuli such as H 2 O 2 (15). Although the importance of SIRT1 in DDR is indisputable, post-translational modification regulation of SIRT1 in DDR has not been fully explored.…”

mentioning

confidence: 99%

Ubiquitinated Sirtuin 1 (SIRT1) Function Is Modulated during DNA Damage-induced Cell Death and Survival

Peng

Yuan

et al. 2015

Journal of Biological Chemistry

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Background: Modulation of histone deacetylase function is crucial for DNA damage-induced cell death and survival. The mechanism of histone deacetylase regulation is poorly understood. Results: Ubiquitination and de-ubiquitination influence sirtuin 1 (SIRT1) histone deacetylase function during DNA damageinduced cell responses. Conclusion: Sirtuin function requires DNA damage-induced SIRT1 ubiquitination. Significance: SIRT1 ubiquitination is a crucial mechanism regulating cell death and survival.

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“…ROS include free radical species, such as hydroxyl radical, lipid radicals, superoxide anion, nitric oxide, and other chemical species with high oxidizing potential, such as hydrogen peroxide, hypochlorous acid, and peroxynitrite (51,52,144). The formation of ROS, originating from a variety of sources such as xanthine oxidases (XO), eNOS uncoupling, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase isoforms, cyclooxygenases, mitochondrial respiration and metal-catalyzed reactions, along with exhaustion of antioxidant enzymes and other antioxidant defenses, results in oxidative and nitrosative stress, a key determinant of endothelial dysfunction (40,51,52,60,128,144).…”

Section: Oxidative Stress and Vascular Dysfunctionmentioning

confidence: 99%

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

D’Onofrio¹,

Servillo²,

Balestrieri³

2018

Antioxidants & Redox Signaling

296

238

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Significance: Oxidative stress represents the common hallmark of pathological conditions associated with cardiovascular disease (CVD), including atherosclerosis, heart failure, hypertension, aging, diabetes, and other vascular system-related diseases. The sirtuin (SIRT) family, comprising seven proteins (SIRT1-SIRT7) sharing a highly conserved nicotinamide adenine dinucleotide (NAD + )-binding catalytic domain, attracted a great attention for the past few years as stress adaptor and epigenetic enzymes involved in the cellular events controlling aging-related disorder, cancer, and CVD. Recent Advances: Among sirtuins, SIRT1 and SIRT6 are the best characterized for their protective roles against inflammation, vascular aging, heart disease, and atherosclerotic plaque development. This latest role has been only recently unveiled for SIRT6. Of interest, in recent years, complex signaling networks controlled by SIRT1 and SIRT6 common to stress resistance, vascular aging, and CVD have emerged. Critical Issues: We provide a comprehensive overview of recent developments on the molecular signaling pathways controlled by SIRT1 and SIRT6, two post-translational modifiers proven to be valuable tools to dampen inflammation and oxidative stress at the cardiovascular level. Future Directions: A deeper understanding of the epigenetic mechanisms through which SIRT1 and SIRT6 act in the signalings responsible for onset and development CVD is a prime scientific endeavor of the upcoming years. Multiple ''omic'' technologies will have widespread implications in understanding such mechanisms, speeding up the achievement of selective and efficient pharmacological modulation of sirtuins for future applications in the prevention and treatment of CVD. Antioxid. Redox Signal. 28, 711-732.

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Deacetylation of the tumor suppressor protein PML regulates hydrogen peroxide-induced cell death

Cited by 42 publications

References 55 publications

Mitochondrial Sirtuins in Cancer: Emerging Roles and Therapeutic Potential

Mitochondrial Sirtuins in Cancer: Emerging Roles and Therapeutic Potential

Ubiquitinated Sirtuin 1 (SIRT1) Function Is Modulated during DNA Damage-induced Cell Death and Survival

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

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