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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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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
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Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...
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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
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DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
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Genetic and Epigenetic Reprogramming of Transposable Elements Drives ecDNA-Mediated Metastatic Prostate Cancer.

Lisanne Mout1, Thaidy Moreno-Rodriguez2, Giacomo Grillo1

  • 1Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.

Biorxiv : the Preprint Server for Biology
|August 20, 2025
PubMed
Summary

Extrachromosomal DNAs (ecDNAs) drive cancer evolution by amplifying oncogenes. In prostate cancer, LINE1 repeats on ecDNAs activate the AR gene, leading to treatment resistance.

Keywords:
ATACBFBChromatinHiCLINE1WGSandrogen receptorcastration resistant prostate cancerecDNAendogenous repetitive elementsenhancerepigeneticepigenomicprostate cancertranscription factorstransposable elementsvariants

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Area of Science:

  • Oncology
  • Genetics
  • Epigenetics

Background:

  • Extrachromosomal DNAs (ecDNAs) facilitate rapid tumor evolution through non-Mendelian replication.
  • Understanding the mechanisms of oncogene amplification in metastatic Castration-Resistant Prostate Cancer (mCRPC) is crucial.

Purpose of the Study:

  • To investigate the role of repeat DNA elements within ecDNAs in driving oncogene overexpression and tumor evolution in mCRPC.
  • To identify specific repeat elements and regulatory mechanisms contributing to AR gene amplification and overexpression.

Main Methods:

  • Integrated analysis of chromatin accessibility, whole-genome sequencing, and Hi-C genome topology data from mCRPC patient cohorts.
  • Identification and characterization of repeat DNA elements co-amplified with oncogenes.

Main Results:

  • A subgroup of mCRPC (20%) exhibits amplified ecDNAs containing accessible LINE1 repeat DNA elements flanking the androgen receptor (AR) gene.
  • These LINE1 elements serve as binding sites for key transcription factors (AR, FOXA1, HOXB13) and form novel 3D chromatin interactions with the AR gene.
  • This regulatory network drives AR overexpression, contributing to resistance against androgen signaling inhibitors.

Conclusions:

  • Epigenetically activated and amplified repeat DNA on ecDNAs are key drivers of oncogene overexpression and tumor evolution.
  • LINE1 elements play a critical role in regulating AR in a subset of mCRPC, promoting therapeutic resistance.