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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Mismatch Repair01:20

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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Selective DNA methylation in cancers controls collateral damage induced by large structural variations.

Vakul Mohanty1, Ogulsheker Akmamedova2, Kakajan Komurov3

  • 1Systems Biology and Physiology Graduate Program, University of Cincinnati, OH, USA.

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Cancer cells with chromosomal instability use DNA methylation to manage toxic gene dosage changes. This mechanism compensates for gene copy number variations, offering potential therapeutic targets for cancer treatment.

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TCGAcomputational cancer biology

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Area of Science:

  • Genomics
  • Cancer Biology
  • Epigenetics

Background:

  • Chromosomal instability is a key feature of human cancers, involving large genomic structural variations.
  • These variations lead to gene dosage changes in co-amplified or co-deleted genes, termed onco-passenger genes, causing collateral stress.

Purpose of the Study:

  • To investigate the regulatory mechanisms compensating for the tumor-toxic effects of onco-passenger gene dosage changes in cancer.
  • To elucidate the role of DNA methylation in uncoupling gene copy number variations from gene expression.

Main Methods:

  • Analysis of gene dosage changes and DNA methylation patterns in chromosomally unstable cancers.
  • Investigating the impact of DNA methylation on the expression of genes within amplified or deleted chromosomal segments.

Main Results:

  • DNA methylation selectively uncouples gene copy number variations from gene expression, mitigating collateral stress.
  • Hypermethylation suppresses overexpression of co-amplified tumor suppressor genes (e.g., TGF-β pathway).
  • Hypomethylation promotes expression of deleted pro-oncogenic genes from the remaining allele.

Conclusions:

  • Selective DNA methylation is a critical tumorigenic mechanism regulating toxic gene copy number imbalance in cancers.
  • Targeting DNA methylation machinery could disrupt compensatory gene expression regulation in chromosomally unstable cancers.
  • Re-activating dormant tumor suppressor pathways via methylation targeting presents a potential therapeutic strategy.