ArticleOncology reports2018
Suppression of Kpnβ1 expression inhibits human breast cancer cell proliferation by abrogating nuclear transport of Her2.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Disruption of ARID1B Recruitment to the Nuclear Pore Complex as a New Anticancer Therapeutic Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Survival-Related Genes on Chromosomes 6 and 17 in Medulloblastoma.International journal of molecular sciences · 2024Article
- Stabilization of KPNB1 by deubiquitinase USP7 promotes glioblastoma progression through the YBX1-NLGN3 axis.Journal of experimental & clinical cancer research : CR · 2024Article
- A mass spectrometry-based approach for the identification of Kpnβ1 binding partners in cancer cells.Scientific reports · 2022Article
- Integrated In Silico Analyses Identify PUF60 and SF3A3 as New Spliceosome-Related Breast Cancer RNA-Binding Proteins.Biology · 2022Article
- KPNB1-mediated nuclear translocation of PD-L1 promotes non-small cell lung cancer cell proliferation via the Gas6/MerTK signaling pathway.Cell death and differentiation · 2021Article
- A Novel Proteomic Method Reveals NLS Tagging of T-DM1 Contravenes Classical Nuclear Transport in a Model of HER2-Positive Breast Cancer.Molecular therapy. Methods & clinical development · 2020Article
- Nuclear ErbB-2: a Novel Therapeutic Target in ErbB-2-Positive Breast Cancer?Hormones & cancer · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer (BC) is one of the most fatal diseases and poses critical health problems worldwide. However, its mechanisms remain unclear. Consequently, there is an urgency to investigate the mechanisms involved in BC initiation and progression and identify novel therapeutics for its prevention and treatment. In this study, we identified karyopherin β-1 (Kpnβ1) as a possible novel therapeutic target for BC. Western blotting was used to evaluate the expression of Kpnβ1 in four pairs of tumorous and adjacent non-tumorous tissues. The results revealed that the protein level of Kpnβ1 was higher in the cancer samples compared with those in the corresponding normal samples. Immunohistochemistry was performed on 140 BC cases and indicated that Kpnβ1 was significantly associated with clinical pathological variables. Kaplan-Meier curve revealed that high expression of Kpnβ1 was related to poor BC patient prognosis. A starvation and re-feeding assay was used to imitate the cell cycle using the SKBR-3 cell line, indicating that Kpnβ1 plays a critical role in cell proliferation. The Cell Counting Kit-8 assay revealed that SKBR-3 cells treated with Kpnβ1-siRNA (siKpnβ1) grew more slowly than the control cells, while flow cytometry revealed that low-Kpnβ1 expressing SKBR-3 cells exhibited increased BC cell apoptosis. Furthermore, the interaction between Kpnβ1 and Her2 was clearly observed by immunoprecipitation, indicating that Kpnβ1-knockdown abrogated nuclear transport of Her2. In summary, our findings revealed that Kpnβ1 is involved in the progression of BC and may be a useful therapeutic target.
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