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Updated: Aug 6, 2026
10:24
Xenopus laevis as a Model to Identify Translation Impairment
Published on: September 27, 2015
XPO1: From basic research to clinical treatment (Review)
Changyan Yang1, Jing Zhu2, Xiang Zheng1
1Department of Genetics, School of Basic Medicine, Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Oncology Reports
|July 24, 2026
Summary
Exportin 1 (XPO1) drives cancer by mislocalizing tumor suppressors. Selective inhibitors of nuclear export (SINE) offer a promising strategy to restore tumor suppressor function and combat cancer.
Area of Science:
- Oncology
- Molecular Biology
- Drug Discovery
Background:
- Exportin 1 (XPO1) is crucial for nuclear export of tumor suppressors and growth mRNAs.
- XPO1 overexpression/hyperactivation in cancer causes tumor suppressor mislocalization, impairing cell cycle arrest, apoptosis, and DNA repair.
- This leads to uncontrolled proliferation, survival, and therapy resistance.
Purpose of the Study:
- To review the molecular mechanisms of XPO1-driven tumorigenesis.
- To examine the rationale for targeting XPO1 therapeutically.
- To focus on the clinical translation of SINE drugs, particularly selinexor, in various cancers.
Main Methods:
- Systematic review of existing literature on XPO1.
- Analysis of molecular mechanisms of XPO1 in cancer.
- Evaluation of clinical trial data for SINE drugs.
- Exploration of combination therapy strategies.
Main Results:
- XPO1 inhibition with SINE drugs is a viable anticancer strategy.
- Selinexor shows potential in hematologic and solid tumors.
- Limitations of monotherapy exist, suggesting combination strategies are crucial.
Conclusions:
- Targeting XPO1 is a promising therapeutic avenue for cancer treatment.
- Combination therapies involving SINE drugs may enhance efficacy.
- Further research and clinical trials are needed to optimize XPO1-targeted therapies.
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