Evidence map›Paper›PMID 42714968›Full record

ArticleCancer discovery2026

Nucleoporins in Cancer: Functional Roles and Therapeutic Opportunities.

Perumalraja Kirthika, Vijayakumar Jawalagatti, Marc Carceles-Cordon, Josep Domingo-Domenech, Veronica Rodriguez-Bravo

Abstract read
In one paragraph

Article in Cancer discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Perumalraja Kirthika *Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-9638-1615
Vijayakumar Jawalagatti *Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0001-8492-5550
Marc Carceles-Cordon *Department of Urology, Mayo Clinic, Rochester, Minnesota.ORCID 0009-0008-6648-215X
Josep Domingo-DomenechDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-7870-7511
Veronica Rodriguez-BravoDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-7363-3672

Funding

Investigating the impact of chromosomal instability on prostate cancer aggressivenessR01CA294563 · NCI · MAYO CLINIC ROCHESTER · PI Veronica Rodriguez-Bravo · 2024 to 2026
$2.4M
Determine the Microphthalmia Transcription Factor (MITF)-regulated cell rewiring mechanisms in lethal prostate cancerR01CA261925 · NCI · THOMAS JEFFERSON UNIVERSITY · PI Josep Maria Domingo-Domenech · 2021 to 2026
$2.2M
Role of Nuclear Pore-Regulated Mechanisms in Prostate Cancer AggressivenessR01CA237398 · NCI · THOMAS JEFFERSON UNIVERSITY · PI RODRIGUEZ-BRAVO, VERONICA · 2020 to 2024
$2.0M
Mechanisms and therapeutic targeting of lethal prostate cancer master regulator transcription factorsR01CA280999 · NCI · MAYO CLINIC ROCHESTER · PI Josep Maria Domingo-Domenech, Veronica Rodriguez-Bravo · 2024 to 2026
$1.6M
Mechanism and therapeutic targeting of castration resistance in SPOP-mutated prostate cancerR01CA285345 · NCI · MAYO CLINIC ROCHESTER · PI Josep Maria Domingo-Domenech, Zhenkun Lou · 2024 to 2026
$1.5M
Mechanism and therapeutic targeting of abnormal androgenesis in CHD1-deficient prostate cancerR01CA286864 · NCI · MAYO CLINIC ROCHESTER · PI Josep Maria Domingo-Domenech, Veronica Rodriguez-Bravo · 2024 to 2026
$1.4M
National Cancer Institute (NCI) R01CA237398National Cancer Institute (NCI) R01CA261925National Cancer Institute (NCI) R01CA280999National Cancer Institute (NCI) R01CA285345National Cancer Institute (NCI) R01CA286864National Cancer Institute (NCI) R01CA294563NCI NIH HHS R01 CA237398NCI NIH HHS R01 CA261925NCI NIH HHS R01 CA280999NCI NIH HHS R01 CA285345NCI NIH HHS R01 CA286864NCI NIH HHS R01 CA294563
6 · The paper itself

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.

Identifiers

PMID42714968
PMCPMC13559546

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.