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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

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Related Experiment Video

Updated: Jul 8, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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Vitamin C enhances co-localization of novel TET1 nuclear bodies with both Cajal and PML bodies in colorectal cancer

Nour El Osmani1,2,3, Corinne Prévostel1,2,4,5, Laurence Picque Lasorsa1,2,4,5

  • 1IRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.

Epigenetics
|April 7, 2024
PubMed
Summary
This summary is machine-generated.

Ten-eleven translocation protein 1 (TET1) localizes to nuclear bodies in colorectal cancer cells. Vitamin C (VitC) influences TET1

Keywords:
5hmCCRCCajal bodiesPML bodiesTET1nuclear bodiespartner proteinsvitamin C

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Cancer Research

Background:

  • Ten-eleven translocation protein 1 (TET1) deregulation is linked to colorectal cancer (CRC) development.
  • Vitamin C (VitC) shows potential in improving CRC prognosis by altering the cancer epigenome and reducing drug resistance.

Purpose of the Study:

  • To characterize TET1-specific subcellular compartments in colonic tumor cells.
  • To evaluate the impact of Vitamin C (VitC) on TET1 compartmentalization within these cells.

Main Methods:

  • Immunofluorescence microscopy to visualize TET1 and 5-hydroxymethylcytosine (5hmC) localization.
  • Co-localization studies to assess interactions between TET1 nuclear bodies (NBs) and other nuclear structures (Cajal bodies, PML bodies).
  • Treatment of HCT116 cells with VitC to observe effects on TET1 and 5hmC distribution.

Main Results:

  • TET1 and its demethylation marker 5hmC were found concentrated in nuclear bodies (NBs) and foci within CRC cell lines (HCT116, Caco-2, HT-29).
  • TET1-NBs were observed to interact with Cajal bodies but not with PML bodies.
  • VitC treatment induced 5hmC foci biogenesis and promoted the formation of active complexes between 5hmC and nuclear components, including Cajal and PML proteins.

Conclusions:

  • This study reveals a novel intracellular localization profile for TET1 and 5hmC in CRC cells.
  • Vitamin C modulates TET1 nuclear body interactions, suggesting a role in epigenetic reprogramming relevant to CRC management.
  • Findings offer new insights into TET1-dependent functions and potential therapeutic strategies for colorectal cancer.