DNA replication stress: oncogenes in the spotlight

Primo, Luiza M. F.; Teixeira, Leonardo K.

doi:10.1590/1678-4685-gmb-2019-0138

Cited by 39 publications

(35 citation statements)

References 141 publications

(52 reference statements)

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“…It is well known that major features of tumors are due to errors in RNA transport and DNA replication, which can lead to cancer and metabolic abnormalities. Abnormal tumor metabolism mainly includes glucose, lipid and amino acid metabolism (52)(53)(54)(55). Additionally, KEGG enrichment analysis of the phosphorylated proteins revealed pathways associated with arrhythmogenic right ventricular cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of phosphoproteins in hepatocellular carcinoma revealed via quantitative analysis of the phosphoproteome

Liu

Zhao

et al. 2020

Oncol Lett

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Section: Discussionmentioning

confidence: 99%

Dysregulation of phosphoproteins in hepatocellular carcinoma revealed via quantitative analysis of the phosphoproteome

Liu

Zhao

et al. 2020

Oncol Lett

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“…DNA replication stress can be induced by different sources, for example, nucleotide pool imbalance or shortage, transcription-replication conflicts, anomalous DNA conformation, difficult-to-replicate loci, or DNA damage caused by endogenous cellular metabolism products, such as reactive oxygen species, exogenous chemical compounds, and UV light and gamma irradiation [88][89][90]. Replication stress is greater in tumor cells, where it is generally caused by either the loss of function of some tumor suppressor genes or deregulated oncogene expression [91].…”

Section: Bp1 Rnf8mentioning

confidence: 99%

Working on Genomic Stability: From the S-Phase to Mitosis

Ovejero

Bueno

Sacristán

2020

Genes

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Fidelity in chromosome duplication and segregation is indispensable for maintaining genomic stability and the perpetuation of life. Challenges to genome integrity jeopardize cell survival and are at the root of different types of pathologies, such as cancer. The following three main sources of genomic instability exist: DNA damage, replicative stress, and chromosome segregation defects. In response to these challenges, eukaryotic cells have evolved control mechanisms, also known as checkpoint systems, which sense under-replicated or damaged DNA and activate specialized DNA repair machineries. Cells make use of these checkpoints throughout interphase to shield genome integrity before mitosis. Later on, when the cells enter into mitosis, the spindle assembly checkpoint (SAC) is activated and remains active until the chromosomes are properly attached to the spindle apparatus to ensure an equal segregation among daughter cells. All of these processes are tightly interconnected and under strict regulation in the context of the cell division cycle. The chromosomal instability underlying cancer pathogenesis has recently emerged as a major source for understanding the mitotic processes that helps to safeguard genome integrity. Here, we review the special interconnection between the S-phase and mitosis in the presence of under-replicated DNA regions. Furthermore, we discuss what is known about the DNA damage response activated in mitosis that preserves chromosomal integrity.

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“…For example, oncogene activation may directly interfere with nucleotide biosynthesis, depleting dNTP pools and ceasing fork progression [64,65]. Defective origin firing and the induction of DNA re-replication are also among the outcomes of replication stress caused by oncogenic stimulus [66,67].…”

Section: Overview Of Dna Replication Stress: How Cells Prevent and Rementioning

confidence: 99%

Protective Mechanisms Against DNA Replication Stress in the Nervous System

Charlier

Martins

2020

Genes

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The precise replication of DNA and the successful segregation of chromosomes are essential for the faithful transmission of genetic information during the cell cycle. Alterations in the dynamics of genome replication, also referred to as DNA replication stress, may lead to DNA damage and, consequently, mutations and chromosomal rearrangements. Extensive research has revealed that DNA replication stress drives genome instability during tumorigenesis. Over decades, genetic studies of inherited syndromes have established a connection between the mutations in genes required for proper DNA repair/DNA damage responses and neurological diseases. It is becoming clear that both the prevention and the responses to replication stress are particularly important for nervous system development and function. The accurate regulation of cell proliferation is key for the expansion of progenitor pools during central nervous system (CNS) development, adult neurogenesis, and regeneration. Moreover, DNA replication stress in glial cells regulates CNS tumorigenesis and plays a role in neurodegenerative diseases such as ataxia telangiectasia (A-T). Here, we review how replication stress generation and replication stress response (RSR) contribute to the CNS development, homeostasis, and disease. Both cell-autonomous mechanisms, as well as the evidence of RSR-mediated alterations of the cellular microenvironment in the nervous system, were discussed.

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DNA replication stress: oncogenes in the spotlight

Cited by 39 publications

References 141 publications

Dysregulation of phosphoproteins in hepatocellular carcinoma revealed via quantitative analysis of the phosphoproteome

Dysregulation of phosphoproteins in hepatocellular carcinoma revealed via quantitative analysis of the phosphoproteome

Working on Genomic Stability: From the S-Phase to Mitosis

Protective Mechanisms Against DNA Replication Stress in the Nervous System

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