Evidence map›Paper›PMID 36593106›Full record

ArticleBMB reports2023

KPNA3 promotes epithelial-mesenchymal transition by regulating TGF-β and AKT signaling pathways in MDA-MB-231, a triple-negative breast cancer cell line.

Jaesung Choi, Jee-Hye Choi, Ho Woon Lee, Dongbeom Seo, Gavaachimed Lkhagvasuren, Jung-Woong Kim, Sang-Beom Seo, Kangseok Lee, Kwang-Ho Lee

Open access · goldAbstract readNews
In one paragraph

Article in BMB reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. The role of KPNA3 in multiple myeloma: implications for targeting nuclear import.Apoptosis : an international journal on programmed cell death · 2026
    Article
  3. Article
  4. 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

9 authors at 2 institutions in 1 country.

Jaesung ChoiDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Jee-Hye ChoiDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Ho Woon LeeDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Dongbeom SeoDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Gavaachimed LkhagvasurenDepartment of Science of Cultural Heritage, Graduate School, Chung-Ang University, Seoul 06974, Korea.
Jung-Woong KimDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Sang-Beom SeoDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Kangseok LeeDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974, Korea.
Kwang-Ho LeeDepartment of Life Science, College of Natural Sciences, Chung-Ang University, Seoul 06974; Department of Science of Cultural Heritage, Graduate School, Chung-Ang University, Seoul 06974, Korea.
Chung-Ang University · KRKorea National University of Cultural Heritage · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Karyopherin-α3 (KPNA3), a karyopherin- α isoform, is intimately associated with metastatic progression via epithelial-mesenchymal transition (EMT). However, the molecular mechanism underlying how KPNA3 acts as an EMT inducer remains to be elucidated. In this report, we identified that KPNA3 was significantly upregulated in cancer cells, particularly in triple-negative breast cancer, and its knockdown resulted in the suppression of cell proliferation and metastasis. The comprehensive transcriptome analysis from KPNA3 knockdown cells indicated that KPNA3 is involved in the regulation of numerous EMTrelated genes, including the downregulation of GATA3 and E-cadherin and the up-regulation of HAS2. Moreover, it was found that KPNA3 EMT-mediated metastasis can be achieved by TGF-β or AKT signaling pathways; this suggests that the novel independent signaling pathways KPNA3-TGF-β-GATA3-HAS2/E-cadherin and KPNA3-AKT-HAS2/E-cadherin are involved in the EMT-mediated progress of TNBC MDA-MB-231 cells. These findings provide new insights into the divergent EMT inducibility of KPNA3 according to cell and cancer type. [BMB Reports 2023; 56(2): 120-125].

Indexed as

alpha KaryopherinsBreast NeoplasmsTriple Negative Breast NeoplasmsCadherinsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleHumansProto-Oncogene Proteins c-aktSignal TransductionTransforming Growth Factor betaalpha KaryopherinsCadherinsKPNA3 protein, humanProto-Oncogene Proteins c-aktTransforming Growth Factor beta

Identifiers

PMID36593106
PMCPMC9978358
OpenAlexW4313454922

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.