AI Article Synopsis
- Exportin-1 (XPO1), known for its role in transporting proteins out of the nucleus, is targeted by new cancer therapies that inhibit this export function.
- Recent research is revealing that XPO1 also plays significant roles in regulating cell division (mitosis) and influencing gene expression patterns (the epigenome).
- As new small molecules are developed to degrade or alter XPO1's function, there's potential to expand its therapeutic applications beyond just cancer treatment.
Article Abstract
Exportin-1 (XPO1), also known as chromosome region maintenance 1 (CRM1), directly binds to and mediates the nuclear export of hundreds of cargo proteins. Blocking nuclear export by the selective inhibitors of nuclear export (SINEs) is a validated therapeutic axis in cancer and an active area of research. However, a growing body of evidence implicates XPO1 in biological functions beyond nuclear export that include the regulation of mitosis and the epigenome. Additionally, new pharmacological classes of small molecules have emerged that degrade XPO1 or induce distinct cellular activity profiles. Here, we discuss the canonical model of nuclear export and XPO1's emergence as an anticancer target. We also spotlight the key evidence for underappreciated XPO1 functions and discuss the use of chemical probes to uncover new cellular roles for XPO1. With these growing trends, the field is poised to extend XPO1 therapeutic targeting to indications beyond oncology.
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| http://dx.doi.org/10.1016/j.tips.2024.11.002 | DOI Listing |
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