XPO1-dependent nuclear export as a target for cancer therapy. Review uri icon

Overview

abstract

  • Cellular homeostasis requires the proper nuclear-cytoplasmic partitioning of large molecules, which is often deregulated in cancer. XPO1 is an export receptor responsible for the nuclear-cytoplasmic transport of hundreds of proteins and multiple RNA species. XPO1 is frequently overexpressed and/or mutated in human cancers and functions as an oncogenic driver. Suppression of XPO1-mediated nuclear export, therefore, presents a unique therapeutic strategy. In this review, we summarize the physiological functions of XPO1 as well as the development of various XPO1 inhibitors and provide an update on the recent clinical trials of the SINE compounds. We also discuss potential future research directions on the molecular function of XPO1 and the clinical application of XPO1 inhibitors.

publication date

  • June 1, 2020

Research

keywords

  • Active Transport, Cell Nucleus
  • Antineoplastic Agents
  • Karyopherins
  • Molecular Targeted Therapy
  • Neoplasm Proteins
  • Receptors, Cytoplasmic and Nuclear

Identity

PubMed Central ID

  • PMC7268335

Scopus Document Identifier

  • 85085910005

Digital Object Identifier (DOI)

  • 10.1186/s13045-020-00903-4

PubMed ID

  • 32487143

Additional Document Info

volume

  • 13

issue

  • 1