Evidence map›Paper›PMID 28427184›Full record

ArticleOncotarget2017

KPNB1-mediated nuclear import is required for motility and inflammatory transcription factor activity in cervical cancer cells.

Tamara Stelma, Virna D Leaner

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  3. Small molecule JRMS modulating importin-β1 chaperone activity as a therapeutic strategy reducing TDP-43 pathology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  17. Karyopherins in cancer.Current opinion in cell biology · 2018
    Review
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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

2 authors at 2 institutions in 1 country.

Tamara StelmaDivision of Medical Biochemistry and Structural Biology, SAMRC Gynaecology Cancer Research Centre, Department of Integrative Biomedical Sciences, Faculty of Health Sciences, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
Virna D LeanerDivision of Medical Biochemistry and Structural Biology, SAMRC Gynaecology Cancer Research Centre, Department of Integrative Biomedical Sciences, Faculty of Health Sciences, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
South African Medical Research Council · ZAUniversity of Cape Town · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Karyopherin β1 is a nuclear import protein involved in the transport of proteins containing a nuclear localisation sequence. Elevated Karyopherin β1 expression has been reported in cancer and transformed cells and is essential for cancer cell proliferation and survival. Transcription factors such as NFĸB and AP-1 contain a nuclear localisation sequence and initiate the expression of multiple factors associated with inflammation and cancer cell biology. Our study investigated the effect of inhibiting nuclear import via Karyopherin β1 on cancer cell motility and inflammatory signaling using siRNA and the novel small molecule, Inhibitor of Nuclear Import-43, INI-43. Inhibition of Karyopherin β1 led to reduced migration and invasion of cervical cancer cells. Karyopherin β1 is essential for the translocation of NFĸB into the nucleus as nuclear import inhibition caused its cytoplasmic retention and decreased transcriptional activity. A similar decrease was seen in AP-1 transcriptional activity upon Karyopherin β1 inhibition. Consequently reduced interleukin-6, interleukin-1 beta, tumour necrosis factor alpha and granulocyte macrophage colony stimulating factor expression, target genes of NFkB and AP-1, was observed. Migration studies inhibiting individual transcription factors suggested that INI-43 may affect a combination of signaling events. Our study provides further evidence that inhibiting KPNB1 has anti-cancer effects and shows promise as a chemotherapeutic target.

Indexed as

Active Transport, Cell Nucleusbeta KaryopherinsCell Line, TumorCell MovementCell NucleusFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansInterleukin-1betaInterleukin-6Neoplasm InvasivenessRNA, Small InterferingTranscription Factor AP-1Tumor Necrosis Factor-alphaUterine Cervical Neoplasmsbeta KaryopherinsIL1B protein, humanIL6 protein, humanInterleukin-1betaInterleukin-6KPNB1 protein, humanRNA, Small InterferingTNF protein, humanTranscription Factor AP-1Tumor Necrosis Factor-alphacervical cancerchemotherapeuticinflammationkaryopherin/importinnuclear import

Identifiers

PMID28427184
PMCPMC5464831
OpenAlexW2592448908

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.