ArticleJournal of ovarian research2015
Novel reversible selective inhibitor of CRM1 for targeted therapy in ovarian cancer.
Article in Journal of ovarian research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Nuclear cathepsin L induces DNA damage by regulating DNA repair factors in ovarian cancer.Oncogene · 2026Article
- Michael Acceptors as Anti-Cancer Compounds: Coincidence or Causality?International journal of molecular sciences · 2024Review
- The nuclear export protein exportin-1 in solid malignant tumours: From biology to clinical trials.Clinical and translational medicine · 2024Review
- Viral Subversion of the Chromosome Region Maintenance 1 Export Pathway and Its Consequences for the Cell Host.Viruses · 2023Review
- RANBP1 (RAN Binding Protein 1): The Missing Genetic Piece in Cancer Pathophysiology and Other Complex Diseases.Cancers · 2023Review
- Article
- Inhibition of XPO-1 Mediated Nuclear Export through the Michael-Acceptor Character of Chalcones.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Crystal structure of human CRM1, covalently modified by 2-mercaptoethanol on Cys528, in complex with RanGTP.Acta crystallographica. Section F, Structural biology communications · 2021Article
- Reversible inhibitor of CRM1 sensitizes glioblastoma cells to radiation by blocking the NF-κB signaling pathway.Cancer cell international · 2020Article
- The past, present, and future of CRM1/XPO1 inhibitors.Stem cell investigation · 2019Review
- Nuclear Export Inhibition for Pancreatic Cancer Therapy.Cancers · 2018Review
- CRM1/XPO1 is associated with clinical outcome in glioma and represents a therapeutic target by perturbing multiple core pathways.Journal of hematology & oncology · 2016Article
- Tissue miR-193b as a Novel Biomarker for Patients with Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Inhibiting cancer cell hallmark features through nuclear export inhibition.Signal transduction and targeted therapyReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOvarian cancer represents the most fatal type of gynecological malignancies. Unfortunately, there are still no effective targeted treatment strategies for ovarian cancer. Overexpression of CRM1 has been correlated with poor prognosis of patients with ovarian cancer.
aimIn this study, we investigated the antitumor effects of a novel reversible inhibitor of CRM1 in ovarian cancer cells.
methodsThe effects of S109 on proliferation was detected by CCK-8, EdU, clonogenic assay. The protein expression were determined by Western blot. The subcellular localization of RanBP1 was analyzed by immunofluorescence microscopy assay.
resultsWe demonstrated that S109 could induce nuclear accumulation of RanBP1, a canonical biomarker for CRM1 inhibition. This effect was clearly reversible in the majority of the cells, whereas the inhibitory effect of LMB could not be reversed. Our data reveal that treatment with S109 results in decrease in proliferation and colonogenic capacity of ovarian cancer cells by arresting cell cycle. Mechanistically, S109 treatment increase the expression of the cyclin-dependent kinase inhibitor p21, while it reduced the expression of cell cycle promoting proteins, Cyclin D1 and Cyclin B. CRM1 level itself was also down-regulated following S109 treatment. Furthermore, the nuclei of cells incubated with S109 accumulated tumor suppressor proteins (Foxo1, p27 and IκB-α). More importantly, Cys528 mutation of CRM1 abolished the ability of S109 to block proliferation of ovarian cancer cells.
conclusionsTogether, our study identifies CRM1 as a valid target in ovarian cancer and provides a basis for the development of S109 in ovarian cancer.
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