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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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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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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
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Mechanistic insights into KDM4A driven genomic instability.

Nicolas L Young1,2, Ruhee Dere2,3

  • 1Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, U.S.A.

Biochemical Society Transactions
|January 25, 2021
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KDM4A, a cancer-associated demethylase, drives genomic instability by altering chromatin methylation and transcriptional regulation. Inhibiting KDM4A offers a promising therapeutic strategy for various cancers.

Keywords:
KDM4Acancerchromatingenome integrity

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Area of Science:

  • Epigenetics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Epigenetic alterations, particularly chromatin methylation, are crucial in cancer development.
  • KDM4A, a histone demethylase, is overexpressed in cancers, correlating with poor prognosis.
  • KDM4A removes H3K9me2/3 and H3K36me3 marks, impacting genome integrity.

Purpose of the Study:

  • To review the role of KDM4A in cancer progression.
  • To explore KDM4A's mechanisms in transcriptional modulation and genomic instability.
  • To highlight KDM4A as a potential therapeutic target.

Main Methods:

  • Literature review focusing on KDM4A's function in cancer.
  • Analysis of KDM4A's enzymatic and non-enzymatic activities.
  • Examination of KDM4A's impact on DNA replication, cell cycle, and checkpoints.

Main Results:

  • KDM4A overexpression promotes cancer through transcriptional dysregulation and genomic instability.
  • KDM4A induces re-replication, activates cell cycle inducers, and impairs checkpoint control.
  • Evidence suggests KDM4A may also affect non-nuclear substrates, contributing to instability.

Conclusions:

  • KDM4A is a key driver of cancer-associated genomic instability.
  • Targeting KDM4A with inhibitors presents a viable therapeutic avenue for cancer treatment.