ReviewMolecular biology reports2025
Targeting the undruggable MYC in cancer: the rationale of using XPO1 inhibitors.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Multi-omics analyses related to mitochondria and ageing in triple-negative breast cancer implicate PYCR1 potentiates tumor progression.Cancer cell international · 2026Article
- Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYC is an important transcription factor involved in physiological processes such as cell growth, proliferation and differentiation. However, aberrant MYC expression has oncogenic-driving potential and is observed in the majority of human cancers. XPO1 is a member of the exportin family of proteins which regulate protein and RNA export from the nucleus to the cytoplasm. XPO1 is aberrantly expressed in cancer, especially with the advancing of the disease. XPO1 inhibition is able to decrease MYC levels through various pathways leading to decreased cancer cell viability. These pathways include other undruggable targets such as p53 and KRAS, DNA damage repair proteins, immune response mediators including IκB, and other transcription factors such as eIF4E. Herein, we describe the potential pathways and mechanisms through which XPO1 inhibition promotes MYC downregulation and subsequent downregulation of its targets. We also describe possible drug combinations with potential clinical applications.
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Registered trials
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