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Related Concept Videos

Epigenetic Regulation01:46

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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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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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Immune Surveillance by NK Cells and Phagocytes01:25

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Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
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meta-Directing Deactivators: –NO2, –CN, –CHO, –⁠CO2R, –COR, –CO2H01:13

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All meta-directing substituents are deactivating groups. These substituents withdraw electrons from the aromatic ring, making the ring less reactive toward electrophilic substitution. For example, the nitration of nitrobenzene is 100,000 times slower than that of benzene because of the deactivating effect of the nitro group. The first step in an electrophilic aromatic substitution is the addition of an electrophile to form a resonance-stabilized carbocation. The energy diagrams for...
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Related Experiment Video

Updated: Feb 1, 2026

Natural Killer NK and CAR-NK Cell Expansion Method using Membrane Bound-IL-21-Modified B Cell Line
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Grainyhead-like-2 confers NK-sensitivity through interactions with epigenetic modifiers.

Ian MacFawn1, Hannah Wilson1, Luke A Selth2

  • 1West Virginia University Cancer Institute, 1 Medical Center Drive, West Virginia University, Morgantown, WV 26505, United States.

Molecular Immunology
|December 4, 2018
PubMed
Summary

Natural Killer (NK) cells are crucial for cancer suppression. This study reveals how the epithelial phenotype, regulated by Grainyhead-like-2 (GRHL2), enhances NK cell activity and killing through epigenetic mechanisms.

Keywords:
EpigeneticGrainyhead-like-2ICAM-1KMT2CKMT2DMesenchymal-to-epithelial transitionNK cellsp300

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Area of Science:

  • Immunology
  • Cancer Biology
  • Epigenetics

Background:

  • Natural Killer (NK) cells are vital in suppressing tumor initiation and metastasis.
  • Carcinomas exhibit heterogeneity, with epithelial, mesenchymal, and hybrid tumor cells, impacting NK cell susceptibility.
  • Grainyhead-like-2 (GRHL2) is a key regulator of the epithelial phenotype, downregulated during Epithelial-Mesenchymal Transition (EMT).

Purpose of the Study:

  • To elucidate the molecular mechanisms linking the epithelial phenotype to NK cell sensitivity.
  • To investigate the role of GRHL2 in modulating NK cell interactions with tumor cells.
  • To identify novel epigenetic pathways connecting epithelial characteristics with NK cell-mediated killing.

Main Methods:

  • Re-expression of GRHL2 in tumor cells to study its effects on NK susceptibility.
  • Analysis of ICAM-1 and interferon response gene expression.
  • Identification of GRHL2-interacting proteins using proteomic approaches.
  • Investigation of epigenetic modifications involving KMT2C, KMT2D, and p300.

Main Results:

  • GRHL2 re-expression increased ICAM-1 expression, enhancing NK cell-target cell interactions and NK cell-mediated killing.
  • Expression of interferon response genes, including ICAM1, inversely correlated with EMT.
  • Two novel GRHL2-interacting proteins, KMT2C and KMT2D (histone methyltransferases), were identified.
  • GRHL2-KMT2C/D interactions and GRHL2's inhibition of p300 promoted mesenchymal-epithelial transition, NK sensitization, and ICAM-1 expression.

Conclusions:

  • GRHL2 plays a critical role in sensitizing epithelial tumor cells to NK cell-mediated killing.
  • Novel epigenetic mechanisms involving KMT2C, KMT2D, and p300 connect the epithelial phenotype to NK cell susceptibility.
  • These findings reveal potentially targetable pathways for enhancing cancer immunotherapy.