The Epigenetic Hallmarks of Cancer DOI
Manel Esteller, Mark A. Dawson, Cigall Kadoch

et al.

Cancer Discovery, Journal Year: 2024, Volume and Issue: 14(10), P. 1783 - 1809

Published: Oct. 4, 2024

Abstract Cancer is a complex disease in which several molecular and cellular pathways converge to foster the tumoral phenotype. Notably, latest iteration of cancer hallmarks, “nonmutational epigenetic reprogramming” was newly added. However, epigenetics, much like genetics, broad scientific area that deserves further attention due its multiple roles initiation, progression, adaptive nature. Herein, we present detailed examination hallmarks affected human cancer, elucidating genes involved, dissecting disrupted landscapes for DNA methylation, histone modifications, chromatin architecture define disease. Significance: characterized by constant evolution, spanning from initial premalignant stages advanced invasive disseminated stages. It pathology able adapt survive amidst hostile microenvironments diverse treatments implemented medical professionals. The more fixed setup genetic structure cannot fully provide transformed cells with tools but rapid plastic nature changes ready task. This review summarizes ecological success our bodies.

Language: Английский

NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential DOI Creative Commons
Na Xie, Lu Zhang, Wei Gao

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2020, Volume and Issue: 5(1)

Published: Oct. 7, 2020

Abstract Nicotinamide adenine dinucleotide (NAD + ) and its metabolites function as critical regulators to maintain physiologic processes, enabling the plastic cells adapt environmental changes including nutrient perturbation, genotoxic factors, circadian disorder, infection, inflammation xenobiotics. These effects are mainly achieved by driving effect of NAD on metabolic pathways enzyme cofactors transferring hydrogen in oxidation-reduction reactions. Besides, multiple -dependent enzymes involved physiology either post-synthesis chemical modification DNA, RNA proteins, or releasing second messenger cyclic ADP-ribose (cADPR) NAADP . Prolonged disequilibrium metabolism disturbs physiological functions, resulting diseases diseases, cancer, aging neurodegeneration disorder. In this review, we summarize recent advances our understanding molecular mechanisms -regulated responses stresses, contribution deficiency various via manipulating cellular communication networks potential new avenues for therapeutic intervention.

Language: Английский

Citations

665

Benefits of Metformin in Attenuating the Hallmarks of Aging DOI Creative Commons
Ameya Kulkarni, Sriram Gubbi, Nir Barzilai

et al.

Cell Metabolism, Journal Year: 2020, Volume and Issue: 32(1), P. 15 - 30

Published: April 24, 2020

Language: Английский

Citations

553

LncRNA‐mediated posttranslational modifications and reprogramming of energy metabolism in cancer DOI Creative Commons

Yue‐Tao Tan,

Jin‐Fei Lin,

Ting Li

et al.

Cancer Communications, Journal Year: 2020, Volume and Issue: 41(2), P. 109 - 120

Published: Oct. 29, 2020

Abstract Altered metabolism is a hallmark of cancer, and the reprogramming energy has historically been considered general phenomenon tumors. It well recognized that long noncoding RNAs (lncRNAs) regulate in cancer. However, lncRNA‐mediated posttranslational modifications metabolic are unclear at present. In this review, we summarized current understanding interactions between alterations cancer‐associated enzymes, transcription factors, other proteins involved pathways. addition, discuss mechanisms through which these contribute to tumor initiation progression, key roles clinical significance functional lncRNAs. We believe an in‐depth cancer can help identify cellular vulnerabilities be exploited for diagnosis therapy.

Language: Английский

Citations

504

Targeting the epigenetic regulation of antitumour immunity DOI
Simon J. Hogg, Paul A. Beavis, Mark A. Dawson

et al.

Nature Reviews Drug Discovery, Journal Year: 2020, Volume and Issue: 19(11), P. 776 - 800

Published: Sept. 14, 2020

Language: Английский

Citations

457

Roles and regulation of histone methylation in animal development DOI
Ashwini Jambhekar, Abhinav Dhall, Yang Shi

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2019, Volume and Issue: 20(10), P. 625 - 641

Published: July 2, 2019

Language: Английский

Citations

446

Non-genetic mechanisms of therapeutic resistance in cancer DOI
Jean‐Christophe Marine, Sarah‐Jane Dawson, Mark A. Dawson

et al.

Nature reviews. Cancer, Journal Year: 2020, Volume and Issue: 20(12), P. 743 - 756

Published: Oct. 8, 2020

Language: Английский

Citations

445

Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer DOI
Andrew W. Caliri, Stella Tommasi, Ahmad Besaratinia

et al.

Mutation Research/Reviews in Mutation Research, Journal Year: 2021, Volume and Issue: 787, P. 108365 - 108365

Published: Jan. 1, 2021

Language: Английский

Citations

408

Kidney fibrosis: from mechanisms to therapeutic medicines DOI Creative Commons

Rongshuang Huang,

Ping Fu, Liang Ma

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: March 17, 2023

Abstract Chronic kidney disease (CKD) is estimated to affect 10–14% of global population. Kidney fibrosis, characterized by excessive extracellular matrix deposition leading scarring, a hallmark manifestation in different progressive CKD; However, at present no antifibrotic therapies against CKD exist. fibrosis identified tubule atrophy, interstitial chronic inflammation and fibrogenesis, glomerulosclerosis, vascular rarefaction. Fibrotic niche, where organ initiates, complex interplay between injured parenchyma (like tubular cells) multiple non-parenchymal cell lineages (immune mesenchymal located spatially within scarring areas. Although the mechanisms are complicated due kinds cells involved, with help single-cell technology, many key questions have been explored, such as what kind renal tubules profibrotic, myofibroblasts originate, which immune how communicate each other. In addition, genetics epigenetics deeper that regulate fibrosis. And reversible nature epigenetic changes including DNA methylation, RNA interference, chromatin remodeling, gives an opportunity stop or reverse therapeutic strategies. More marketed (e.g., RAS blockage, SGLT2 inhibitors) developed delay progression recent years. Furthermore, better understanding also favored discover biomarkers fibrotic injury. review, we update advances mechanism summarize novel treatment for CKD.

Language: Английский

Citations

274

N7-Methylguanosine tRNA modification enhances oncogenic mRNA translation and promotes intrahepatic cholangiocarcinoma progression DOI Creative Commons
Zihao Dai, Hai‐Ning Liu, Junbin Liao

et al.

Molecular Cell, Journal Year: 2021, Volume and Issue: 81(16), P. 3339 - 3355.e8

Published: Aug. 1, 2021

Language: Английский

Citations

218

Taurine deficiency as a driver of aging DOI Open Access
Parminder Singh, Kishore Gollapalli, Stefano Mangiola

et al.

Science, Journal Year: 2023, Volume and Issue: 380(6649)

Published: June 8, 2023

Aging is associated with changes in circulating levels of various molecules, some which remain undefined. We find that concentrations taurine decline aging mice, monkeys, and humans. A reversal this through supplementation increased the health span (the period healthy living) life mice monkeys. Mechanistically, reduced cellular senescence, protected against telomerase deficiency, suppressed mitochondrial dysfunction, decreased DNA damage, attenuated inflammaging. In humans, lower correlated several age-related diseases after acute endurance exercise. Thus, deficiency may be a driver because its increases worms, rodents, primates worms rodents. Clinical trials humans seem warranted to test whether might drive

Language: Английский

Citations

217