<p>Exportin-1 (XPO1) is fundamental in the regulation of nuclear-to-cytoplasm transportation. XPO1 has the ability to transport hundreds of proteins and several different types of mRNAs responsible for proper cellular biology. Deregulation of the XPO1 transportation system aberrantly translocates transcription factors promoting the pathogenesis of diseases including cancer. However, XPO1 has transport-independent functions that involve epigenetic modifications. XPO1 associates with chromatin, recruiting oncogenic fusion proteins to target genes affecting chromatin structure and function. That intriguing association also affects transcriptional activation resulting in oncogenesis. XPO1 also regulates other epigenetic pathways and is epigenetically regulated as well. Herein, we report most recent findings on that topic, and we discuss the mechanisms and the consequences of normal and aberrant XPO1 association with the epigenetic marks.</p>

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Exportin-1 and epigenetic modifications interaction: more than nuclear transport

  • Leonidas Benetatos,
  • Eleftheria Hatzimichael,
  • Eleni Kapsali

摘要

Exportin-1 (XPO1) is fundamental in the regulation of nuclear-to-cytoplasm transportation. XPO1 has the ability to transport hundreds of proteins and several different types of mRNAs responsible for proper cellular biology. Deregulation of the XPO1 transportation system aberrantly translocates transcription factors promoting the pathogenesis of diseases including cancer. However, XPO1 has transport-independent functions that involve epigenetic modifications. XPO1 associates with chromatin, recruiting oncogenic fusion proteins to target genes affecting chromatin structure and function. That intriguing association also affects transcriptional activation resulting in oncogenesis. XPO1 also regulates other epigenetic pathways and is epigenetically regulated as well. Herein, we report most recent findings on that topic, and we discuss the mechanisms and the consequences of normal and aberrant XPO1 association with the epigenetic marks.