Evidence map›Paper›PMID 35196484›Full record

ArticleCell reports2022

Nucleoporin-93 reveals a common feature of aggressive breast cancers: robust nucleocytoplasmic transport of transcription factors.

Nishanth Belugali Nataraj, Ashish Noronha, Joo Sang Lee, Soma Ghosh, Harsha Raj Mohan Raju, Arunachalam Sekar, Binyamin Zuckerman, Moshit Lindzen, Emilio Tarcitano, Swati Srivastava and 12 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  5. Dual targeting of AMRC12 andTheranostics · 2026
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  18. Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023
    Review
  19. Article
  20. Article
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

22 authors at 5 institutions in 3 countries.

Nishanth Belugali NatarajDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Ashish NoronhaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Joo Sang LeeCancer Data Science Lab, National Cancer Institute, NIH, Rockville, MD, USA.
Soma GhoshDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Harsha Raj Mohan RajuDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Arunachalam SekarDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Binyamin ZuckermanDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Moshit LindzenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Emilio TarcitanoDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Swati SrivastavaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Michael SelitrennikDepartment of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Ido LivnehTechnion Integrated Cancer Center (TICC) and the Rappaport Faculty of Medicine and Research Institute, Technion-Israel Institute of Technology, Haifa, Israel.
Diana Drago-GarciaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Oscar RuedaCancer Research UK Cambridge Institute, University of Cambridge and the Cambridge Cancer Centre, Department of Oncology, Cambridge, UK.
Carlos CaldasCancer Research UK Cambridge Institute, University of Cambridge and the Cambridge Cancer Centre, Department of Oncology, Cambridge, UK.
Sima LevDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Tamar GeigerDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel; Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Aaron CiechanoverTechnion Integrated Cancer Center (TICC) and the Rappaport Faculty of Medicine and Research Institute, Technion-Israel Institute of Technology, Haifa, Israel.
Igor UlitskyDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Rony SegerDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Eytan RuppinCancer Data Science Lab, National Cancer Institute, NIH, Rockville, MD, USA.
Yosef YardenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel. Electronic address: yosef.yarden@weizmann.ac.il.
Weizmann Institute of Science · ILNational Cancer Institute · USTechnion – Israel Institute of Technology · ILTel Aviv University · ILUniversity of Cambridge · GB

Funding

Discovery of genetic interactions in cancerZIABC011802 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RUPPIN, EYTAN · 2018 to 2025
$19.6M
Next generation strategies to intercept ErbB signalingR37CA072981 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI YARDEN, YOSEF · 2005 to 2014
$2.3M
LATERAL VERSUS VERTICAL SIGNALING BY ERBB2 ONCOPROTEINR01CA072981 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI YARDEN, YOSEF NONE · 1997 to 2004
$953k
Cancer Research UK 16942Cancer Research UK 29567NCI NIH HHS R01 CA072981NCI NIH HHS R37 CA072981
6 · The paper itself

Abstract

By establishing multi-omics pipelines, we uncover overexpression and gene copy-number alterations of nucleoporin-93 (NUP93), a nuclear pore component, in aggressive human mammary tumors. NUP93 overexpression enhances transendothelial migration and matrix invasion in vitro, along with tumor growth and metastasis in animal models. These findings are supported by analyses of two sets of naturally occurring mutations: rare oncogenic mutations and inactivating familial nephrotic syndrome mutations. Mechanistically, NUP93 binds with importins, boosts nuclear transport of importins' cargoes, such as β-catenin, and activates MYC. Likewise, NUP93 overexpression enhances the ultimate nuclear transport step shared by additional signaling pathways, including TGF-β/SMAD and EGF/ERK. The emerging addiction to nuclear transport exposes vulnerabilities of NUP93-overexpressing tumors. Congruently, myristoylated peptides corresponding to the nuclear translocation signals of SMAD and ERK can inhibit tumor growth and metastasis. Our study sheds light on an emerging hallmark of advanced tumors, which derive benefit from robust nucleocytoplasmic transport.

Indexed as

Breast NeoplasmsNuclear Pore Complex ProteinsActive Transport, Cell NucleusAnimalsFemaleHumansNuclear PoreTranscription FactorsNuclear Pore Complex ProteinsNup93 protein, humanTranscription Factorsbreast cancercancer hallmarkEGF/ERKimportinmetastasisnuclear porenuclear transportTGF-β/SMADtranscription factorWNT/β-catenin

Identifiers

PMID35196484
PMCPMC8957480
OpenAlexW4214537301

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.