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The DNA Replication Fork01:02

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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
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DNA replication stress: oncogenes in the spotlight.

Luiza M F Primo1, Leonardo K Teixeira1

  • 1Group of Cell Cycle Control, Program of Immunology and Tumor Biology. Brazilian National Cancer Institute (INCA), Rio de Janeiro, RJ, Brazil.

Genetics and Molecular Biology
|January 14, 2020
PubMed
Summary

Oncogene activation disrupts DNA replication, causing genomic instability crucial for cancer development. This review details how oncogenes like RAS and MYC induce replication stress, promoting genetic alterations in carcinogenesis.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Biology

Background:

  • Precise DNA replication is vital for genome stability and accurate transmission of genetic information.
  • DNA replication stress, characterized by slowed replication fork progression, can arise from various cellular insults.
  • Oncogene activation is a known driver of genomic instability, often through interference with DNA replication.

Purpose of the Study:

  • To review the role of oncogenes in inducing DNA replication stress.
  • To elucidate the molecular mechanisms by which oncogenes disrupt DNA replication.
  • To highlight the contribution of oncogene-induced replication stress to genomic instability and human carcinogenesis.

Main Methods:

  • Literature review focusing on oncogenes and DNA replication stress.
  • Analysis of molecular mechanisms linking oncogene activation to replication fork dynamics.
  • Synthesis of evidence connecting replication stress to genomic instability in cancer.

Main Results:

  • Specific oncogenes including RAS, MYC, Cyclin E, MDM2, and BCL-2 were identified as inducers of DNA replication stress.
  • These oncogenes interfere with DNA replication through diverse molecular pathways.
  • Oncogene-induced replication stress is a significant contributor to the genomic instability observed in human cancers.

Conclusions:

  • Oncogene activation is a critical factor in initiating DNA replication stress.
  • Understanding these mechanisms provides insights into cancer development and potential therapeutic targets.
  • Targeting oncogene-induced replication stress may offer strategies to combat genomic instability in cancer.