An Epigenetic Role of Mitochondria in Cancer

Liu, Yu’e; Chen, Chao; Wang, Xinye; Sun, Yongqiang; Zhang, Jin; Chen, Juxiang; Shi, Yufeng

doi:10.3390/cells11162518

Cited by 74 publications

(69 citation statements)

References 535 publications

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“…This gene codes for the p53 protein, which is a transcription factor that prevents abnormal proliferation and division of cells ( 2 ). Recent research has found that TP53 is involved in the regulation of various types of programmed cell death (PCD), which include apoptosis ( 3 ), autophagy ( 4 , 5 ), pyroptosis ( 6 ), and ferroptosis ( 7 ), and pathways for generation of reactive oxygen species (ROS) ( 8 – 10 ). For example, p53 promotes apoptosis by upregulating apoptosis-related proteins in order to stabilize the organism ( 11 , 12 ).…”

Section: Tp53 and Programmed Cell Death In Cancermentioning

confidence: 99%

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Current insights into the regulation of programmed cell death by TP53 mutation in cancer

Sai

Zhou

et al. 2022

Front. Oncol.

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Gene mutation is a complicated process that influences the onset and progression of cancer, and the most prevalent mutation involves the TP53 gene. One of the ways in which the body maintains homeostasis is programmed cell death, which includes apoptosis, autophagic cell death, pyroptosis, ferroptosis, NETosis, and the more recently identified process of cuprotosis. Evasion of these cell deaths is a hallmark of cancer cells, and our elucidation of the way these cells die helps us better understands the mechanisms by which cancer arises and provides us with more ways to treat it.Studies have shown that programmed cell death requires wild-type p53 protein and that mutations of TP53 can affect these modes of programmed cell death. For example, mutant p53 promotes iron-dependent cell death in ferroptosis and inhibits apoptotic and autophagic cell death. It is clear that TP53 mutations act on more than one pathway to death, and these pathways to death do not operate in isolation. They interact with each other and together determine cell death. This review focuses on the mechanisms via which TP53 mutation affects programmed cell death. Clinical investigations of TP53 mutation and the potential for targeted pharmacological agents that can be used to treat cancer are discussed.

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Section: Tp53 and Programmed Cell Death In Cancermentioning

confidence: 99%

“…(6), and ferroptosis (7), and pathways for generation of reactive oxygen species (ROS) (8)(9)(10). For example, p53 promotes apoptosis by upregulating apoptosis-related proteins in order to stabilize the organism (11,12).…”

mentioning

confidence: 99%

Current insights into the regulation of programmed cell death by TP53 mutation in cancer

Sai

Zhou

et al. 2022

Front. Oncol.

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“…Cancer, one of the most frequent diseases worldwide, are characterized by continuous cell proliferation and dysregulation of the cell cycle. This outlines the importance of chemotherapeutic agents to the modulate cell cycle and/or apoptosis [ 102 , 103 ]. The approach for understanding means of PPAR-γ activation has gained considerable momentum in recent years which is found to be expressed in a variety of cancer cells.…”

Section: Ppar-γ Agonists In Various Diseasesmentioning

confidence: 99%

PPAR-γ Partial Agonists in Disease-Fate Decision with Special Reference to Cancer

Ballav

Biswas

Sahu

et al. 2022

Cells

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Peroxisome proliferator-activated receptor-γ (PPAR-γ) has emerged as one of the most extensively studied transcription factors since its discovery in 1990, highlighting its importance in the etiology and treatment of numerous diseases involving various types of cancer, type 2 diabetes mellitus, autoimmune, dermatological and cardiovascular disorders. Ligands are regarded as the key determinant for the tissue-specific activation of PPAR-γ. However, the mechanism governing this process is merely a contradictory debate which is yet to be systematically researched. Either these receptors get weakly activated by endogenous or natural ligands or leads to a direct over-activation process by synthetic ligands, serving as complete full agonists. Therefore, fine-tuning on the action of PPAR-γ and more subtle modulation can be a rewarding approach which might open new avenues for the treatment of several diseases. In the recent era, researchers have sought to develop safer partial PPAR-γ agonists in order to dodge the toxicity induced by full agonists, akin to a balanced activation. With a particular reference to cancer, this review concentrates on the therapeutic role of partial agonists, especially in cancer treatment. Additionally, a timely examination of their efficacy on various other disease-fate decisions has been also discussed.

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“…Biomarkers of lipid peroxidation including elevated levels of TBARS were significant significantly higher in the plasma of patients with T2D in comparison to healthy subjects [ 13 ]. Beyond its implication during the development of T2D, elevated biomarkers of lipid peroxidation have been crucial in highlighting the pathological role of oxidative stress during the pathogenesis of other conditions, including cerebral vascular disease [ 14 , 15 ], obesity-driven cancer [ 16 , 17 , 18 ], and age-related dementia [ 19 ]. Thus, it is essential to recognize antioxidant therapies as a potential strategy to combat lipid peroxidation and oxidative stress during the development of diverse chronic diseases, including T2D [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Detrimental Effects of Lipid Peroxidation in Type 2 Diabetes: Exploring the Neutralizing Influence of Antioxidants

et al. 2022

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Lipid peroxidation, including its prominent byproducts such as malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE), has long been linked with worsened metabolic health in patients with type 2 diabetes (T2D). In fact, patients with T2D already display increased levels of lipids in circulation, including low-density lipoprotein-cholesterol and triglycerides, which are easily attacked by reactive oxygen molecules to give rise to lipid peroxidation. This process severely depletes intracellular antioxidants to cause excess generation of oxidative stress. This consequence mainly drives poor glycemic control and metabolic complications that are implicated in the development of cardiovascular disease. The current review explores the pathological relevance of elevated lipid peroxidation products in T2D, especially highlighting their potential role as biomarkers and therapeutic targets in disease severity. In addition, we briefly explain the implication of some prominent antioxidant enzymes/factors involved in the blockade of lipid peroxidation, including termination reactions that involve the effect of antioxidants, such as catalase, coenzyme Q10, glutathione peroxidase, and superoxide dismutase, as well as vitamins C and E.

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An Epigenetic Role of Mitochondria in Cancer

Cited by 74 publications

References 535 publications

Current insights into the regulation of programmed cell death by TP53 mutation in cancer

Current insights into the regulation of programmed cell death by TP53 mutation in cancer

PPAR-γ Partial Agonists in Disease-Fate Decision with Special Reference to Cancer

Detrimental Effects of Lipid Peroxidation in Type 2 Diabetes: Exploring the Neutralizing Influence of Antioxidants

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