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RNA Research and Splicing · Journal article
Cancer Discovery · September 9, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review of nucleoporins and the nuclear pore complex in cancer, proposing that NUP dysregulation contributes to tumor pathogenesis through disruption of nucleocytoplasmic transport, chromatin regulation, and genome stability. The source identifies NUPs and NPC-regulated pathways as potential pharmacological targets, including via molecular glues and inhibitors of transport and epigenomic signaling, but presents no new experimental or clinical evidence to support efficacy or safety.
Journal article.
NUPs play fundamental roles in maintaining cellular fitness through regulation of nucleocytoplasmic transport, chromatin activity, and genome stability. Tumor-driven co-option of NUP-regulated functions contributes to pathogenesis of multiple malignancies. NPC-regulated mechanisms can be pharmacologically targeted using clinical-grade molecular glues for selective NUP degradation and inhibitors of NPC-regulated epigenomic/transcriptomic signaling and nucleocytoplasmic transport.
Therapeutic opportunities are proposed conceptually; no phase of drug development, toxicity, or clinical response is documented. NPC-regulated mechanisms can be pharmacologically targeted using clinical-grade molecular glues for selective NUP degradation and inhibitors of NPC-regulated epigenomic/transcriptomic signaling and nucleocytoplasmic transport.
The source did not state who this applies to in practice.
A narrative review synthesizing mechanistic evidence and therapeutic concepts without reporting new experimental data, clinical trials, or original empirical results.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Abstract The nuclear pore complex (NPC) and its building-block proteins, nucleoporins (NUP), play fundamental roles in maintaining cellular fitness by regulating nucleocytoplasmic transport, chromatin and transcriptional activity, and genome stability. These core biological processes are critical for cancer cells, and thus, tumor-driven co-option of NUP-regulated functions has emerged as an important mechanism contributing to the pathogenesis of multiple malignancies. This review discusses how NUP dysregulation mechanistically contributes to tumor initiation and progression and how these insights open opportunities for innovative anticancer therapies, including using clinical-grade molecular glues that induce selective NUP degradation and pharmacologically inhibiting NPC-regulated epigenomic/transcriptomic signaling and nucleocytoplasmic transport. Significance: Recent studies demonstrate that NUPs play fundamental roles in cancer pathogenesis by dysregulating key NPC functions and driving tumorigenesis and disease progression. NUPs and NPC-regulated mechanisms can be pharmacologically targeted, providing a strong rationale for developing much-needed innovative therapeutic strategies to combat cancer.
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