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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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Non-LTR Retrotransposons03:18

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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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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Induced Pluripotent Stem Cells01:06

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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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Updated: Aug 18, 2025

LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles
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LINE-1 Methylation Analysis in Mesenchymal Stem Cells Treated with Osteosarcoma-Derived Extracellular Vesicles

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An Epigenetic LINE-1-Based Mechanism in Cancer.

Patrizia Lavia1, Ilaria Sciamanna2, Corrado Spadafora3

  • 1Institute of Molecular Biology and Pathology (IBPM), CNR Consiglio Nazionale delle Ricerche, c/o Department of Biology and Biotechnology, Sapienza University of Rome, 00185 Rome, Italy.

International Journal of Molecular Sciences
|December 11, 2022
PubMed
Summary
This summary is machine-generated.

Cancer arises from stress-induced epigenetic changes, including the upregulation of long interspersed nuclear element 1 (LINE-1) retrotransposons. This leads to genome plasticity, reprogramming gene expression, and reactivating embryonic profiles, driving cancer progression.

Keywords:
LINE-1 retrotransposonsRT inhibitorsautophagycancer genesis and progressionchromatinembryogenesisgenome expressionnuclear laminareverse transcriptase (RT)

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RNA Next-Generation Sequencing and a Bioinformatics Pipeline to Identify Expressed LINE-1s at the Locus-Specific Level
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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • Decades of research have revealed cancer's complexity, multifactoriality, and heterogeneity.
  • Genome plasticity is increasingly recognized as a key factor in cancer biology.
  • Existing knowledge highlights the need for novel insights into cancer onset and progression.

Purpose of the Study:

  • To propose a novel stress-responsive epigenetic mechanism driving cancer onset and progression.
  • To elucidate the role of long interspersed nuclear element 1 (LINE-1) retrotransposons in cancer development.
  • To connect genome plasticity, epigenetic reprogramming, and cancer phenotypes.

Main Methods:

  • The study proposes a theoretical framework based on existing literature and molecular mechanisms.
  • It integrates concepts of epigenetics, genome damage, nuclear architecture, and cellular processes like autophagy.
  • Focuses on the convergence of specific molecular events leading to cancer phenotypes.

Main Results:

  • Cancer onset and progression are driven by a stress-responsive epigenetic mechanism.
  • Upregulation of LINE-1 retrotransposons is a key component, increasing genome plasticity.
  • This leads to reprogramming of global gene expression, including reactivation of embryonic transcription profiles.

Conclusions:

  • Cancer phenotypes emerge from unscheduled reactivation of embryonic gene expression patterns.
  • De-differentiation and aberrant proliferation in differentiated cells are triggered by this reprogramming.
  • The degree of malignancy is dependent on stress intensity and LINE-1 response levels.