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Correction of aberrant imprinting of IGF2 in human tumors by nuclear transfer-induced epigenetic reprogramming

Hui Ling Chen1, Tao Li, Xin Wen Qiu

  • 1Medical Service, VA Palo Alto Health Care System, Palo Alto, CA, USA.

The EMBO Journal
|November 4, 2006
PubMed

Insights

Loss of genomic imprinting of insulin-like growth factor II (IGF2) can be corrected by reprogramming tumor cell nuclei. This suggests that epigenetic abnormalities in cancer may be reversible through in vitro methods.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Genomic Imprinting

Background:

  • Loss of genomic imprinting of insulin-like growth factor II (IGF2) is a common characteristic of human cancers.
  • This aberrant epigenotype contributes to tumor development and progression.

Purpose of the Study:

  • To investigate the potential for correcting the loss of IGF2 imprinting in human tumor cells.
  • To explore in vitro reprogramming as a method to restore normal epigenetic patterns in cancer.

Main Methods:

  • Nuclear transfer of human tumor cell nuclei into enucleated fibroblasts (mouse and human) with normal IGF2 imprinting.
  • Analysis of IGF2 expression patterns in reconstructed diploid and tetraploid hybrid cells.
  • Inhibition of protein synthesis using cycloheximide to identify trans-acting imprinting factors.

Main Results:

  • Abnormal biallelic IGF2 expression in tumor nuclei was transiently corrected to monoallelic expression in reconstructed diploid cells.
  • Normal IGF2 imprinting was permanently restored in the tumor genome within tetraploid hybrid cells.
  • Inhibition of protein synthesis in normal fibroblasts led to loss of IGF2 imprinting, indicating the presence of trans-acting factors.

Conclusions:

  • In vitro reprogramming can correct abnormal tumor epigenotypes, specifically the loss of IGF2 imprinting.
  • Loss of imprinting in tumors is linked to the inactivation or mutation of non-CTCF trans-acting imprinting factors.
  • These findings suggest potential therapeutic strategies targeting epigenetic defects in cancer.

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