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Related Concept Videos

Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Epigenetic Regulation01:37

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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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Adaptive Mechanisms in Cancer Cells02:53

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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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Regulation of Angiogenesis and Blood Supply01:24

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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Updated: Jul 9, 2025

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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Epigenetic remodelling under hypoxia.

Roxane Verdikt1, Bernard Thienpont2

  • 1Institute for Society and Genetics, University of California, Los Angeles, Los Angeles, CA, USA; Department of Human Genetics, KU Leuven, Leuven, Belgium; KU Leuven Institute for Single Cell Omics (LISCO), KU Leuven, Leuven, Belgium.

Seminars in Cancer Biology
|November 29, 2023
PubMed
Summary
This summary is machine-generated.

Hypoxia, a lack of oxygen in tumors, drives cancer malignancy and treatment resistance. Epigenetic mechanisms are key to how cancer cells adapt to hypoxia, influencing gene regulation and metabolic reprogramming for therapeutic development.

Keywords:
Cancer programsEpigeneticsTumour hypoxia

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Last Updated: Jul 9, 2025

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Hypoxia is a common characteristic of solid tumors.
  • Tumor hypoxia promotes cancer progression, metastasis, and resistance to therapy.
  • Epigenetic mechanisms are critical for cancer cell adaptation to hypoxic conditions.

Purpose of the Study:

  • To review the current literature on the epigenetic control of gene programs in hypoxic cancer cells.
  • To highlight common themes and features of epigenetic remodeling in response to hypoxia.
  • To discuss the relevance of these findings for developing novel therapeutic strategies.

Main Methods:

  • Literature review of studies on epigenetic regulation in hypoxic cancer cells.
  • Analysis of common epigenetic modifications and their associated gene expression changes.
  • Integration of findings with known hypoxia-sensitive transcription factors and metabolic reprogramming.

Main Results:

  • Epigenetic mechanisms are crucial for sensing oxygen levels and adapting to chronic hypoxia.
  • A complex network involving epigenetic regulation, transcription factors, and metabolic reprogramming governs hypoxic cancer cell programs.
  • Common themes in epigenetic remodeling facilitate tumor adaptation and progression under hypoxia.

Conclusions:

  • Epigenetic control is a central mechanism in hypoxic cancer cell adaptation.
  • Understanding these epigenetic changes offers potential for developing targeted cancer therapies.
  • Targeting epigenetic modifications in hypoxic tumors may overcome treatment resistance.