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Related Concept Videos

DNA Replication02:40

DNA Replication

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DNA replication involves the separation of the two strands of the double helix, with each strand serving as a template from which the new complementary strand is copied.  After replication, each double-stranded DNA includes one parental or “old” strand and one “new” strand. This is known as semiconservative replication. The resulting DNA molecules have the same sequence and are divided equally into the two daughter cells.
Replication in Prokaryotes
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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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DNA Helicases00:55

DNA Helicases

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DNA unwinding helicase enzymes are a type of motor protein. Motor proteins can translocate along filaments or polymers using energy generated from ATP hydrolysis. Helicases are involved in all the important cellular processes where DNA unwinding is required, such as DNA replication, repair, recombination, and transcription. They are present in all living organisms, but vary in their structure, function, and mechanism of action. For example, in prokaryotes, DnaB helicase binds and translocates...
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S-Cdk Initiates DNA Replication02:38

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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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Chromosome Replication02:31

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Before a cell can divide, it must accurately replicate all of its chromosomes, including the DNA and its associated histone and non-histone proteins.  This process begins at numerous origins of replication during the S phase of the cell cycle in each of a cell’s chromosomes simultaneously. Certain nucleotides can act as origins of replication, but these sequences are not well defined - especially in complex, multi-cellular, eukaryotic species. The length of DNA that spans an origin...
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Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
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DNA Replication Vulnerabilities Render Ovarian Cancer Cells Sensitive to Poly(ADP-Ribose) Glycohydrolase Inhibitors.

Nisha Pillay1, Anthony Tighe1, Louisa Nelson1

  • 1Division of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, 555 Wilmslow Road, Manchester M20 4GJ, UK.

Cancer Cell
|March 20, 2019
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Summary

Poly(ADP-ribose) glycohydrolase (PARG) inhibitors show promise for ovarian cancer treatment. These inhibitors target DNA replication vulnerabilities and offer a complementary strategy to poly(ADP-ribose) polymerase (PARP) inhibitors.

Keywords:
DNA damageHGSOCPARGPARPTIMELESSreplication catastropheγH2AX

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Poly(ADP-ribose) polymerase (PARP) inhibitors are effective in BRCA-mutant ovarian cancer.
  • Limited efficacy in the broader ovarian cancer population due to low BRCA mutation rates.
  • Need for novel therapeutic strategies beyond PARP inhibition.

Purpose of the Study:

  • To investigate the therapeutic potential of poly(ADP-ribose) glycohydrolase (PARG) inhibitors in ovarian cancer.
  • To identify mechanisms of sensitivity and resistance to PARG inhibitors.
  • To explore combination strategies with existing therapies.

Main Methods:

  • Screening of ovarian cancer cell lines and ex vivo patient-derived models with a PARG inhibitor.
  • Analysis of DNA replication dynamics and fork stalling.
  • Synthetic lethality studies with CHK1 inhibitors.

Main Results:

  • A subset of ovarian cancer models demonstrated sensitivity to PARG inhibitors.
  • Sensitivity was linked to DNA replication vulnerabilities and persistent fork stalling.
  • PARG inhibition showed synthetic lethality with CHK1 inhibitors, expanding the sensitive population.
  • PARG and PARP inhibitor sensitivity were mutually exclusive.

Conclusions:

  • PARG inhibitors represent a promising therapeutic strategy for ovarian cancer.
  • PARG inhibitors can overcome resistance to PARP inhibitors by targeting distinct vulnerabilities.
  • Combination therapy with CHK1 inhibitors may broaden the applicability of PARG inhibitors.