ArticleOncotarget2016
Selinexor, a Selective Inhibitor of Nuclear Export (SINE) compound, acts through NF-κB deactivation and combines with proteasome inhibitors to synergistically induce tumor cell death.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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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.
Who cites it
92 citing papers in PubMed, 129 citations in OpenAlex.
- Selinexor combined with R-CHOP achieved a high response rate in newly diagnosed double/triple-hit lymphoma.Blood advances · 2026Trial
- Selinexor Plus Ruxolitinib in Janus Kinase Inhibitor-Naïve Myelofibrosis: Phase III SENTRY Trial.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026Trial
- Once weekly selinexor, carfilzomib and dexamethasone in carfilzomib non-refractory multiple myeloma patients.British journal of cancer · 2022Trial
- A Phase II Study of the Efficacy and Safety of Oral Selinexor in Recurrent Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- Selinexor, bortezomib, and dexamethasone versus bortezomib and dexamethasone in previously treated multiple myeloma: Outcomes by cytogenetic risk.American journal of hematology · 2021Trial
- Trial
- Selective Inhibition of Nuclear Export With Oral Selinexor for Treatment of Relapsed or Refractory Multiple Myeloma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Trial
- XPO1-dependent nuclear export regulates NS3 localization and promotes DENV-2 replication through mitochondrial remodeling and interferon suppression.Nucleus (Austin, Tex.) · 2026Article
- XPO1: From basic research to clinical treatment (Review).Oncology reports · 2026Review
- Targeting nuclear export and Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signalling in myelofibrosis: A novel combinatorial strategy that impacts intrinsic and microenvironment-related pathways.British journal of haematology · 2026Article
- Selinexor plus tislelizumab in patients with relapsed/refractory natural killer/T-cell lymphoma after failure of PD-1 blockade: the phase 1b TOUCH trial.The oncologist · 2026Article
- Selinexor for myelofibrosis or a drug in search of a disease?Blood cancer journal · 2026Article
- Selinexor plus ruxolitinib in JAK inhibitor-naïve patients with myelofibrosis: a multicenter, open-label, phase 1 study.Blood advances · 2026Article
- Multidimensional Regulatory Network and Spatiotemporal Specificity of FOXO Transcription Factors in Digestive System Tumors: Recent Advances.International journal of molecular sciences · 2026Review
- Integration of Network Pharmacology and Molecular Docking Together with an In Vitro Nitric Oxide Inhibition for the Insight for Antipyretic Effects of Benjalokawichian, the Thai Traditional Polyherbal Remedy.International journal of molecular sciences · 2026Article
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Refining the role of selinexor in multiple myeloma: strategic use in a shifting treatment landscape.ESMO open · 2026Review
- Nuclear-Cytoplasmic Axis in Cancer: From Protein Mislocalization to Anticancer Drug Resistance.Oncology research · 2026Review
- Current Status of Molecularly Targeted Therapeutics in Blood Cancers.International journal of molecular sciences · 2025Review
- A phase IIb study of selinexor in combination with daratumumab in patients with daratumumab-refractory multiple myeloma.Haematologica · 2025Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear export protein, exportin-1 (XPO1/CRM1), is overexpressed in many cancers and correlates with poor prognosis. Selinexor, a first-in-class Selective Inhibitor of Nuclear Export (SINE) compound, binds covalently to XPO1 and blocks its function. Treatment of cancer cells with selinexor results in nuclear retention of major tumor suppressor proteins and cell cycle regulators, leading to growth arrest and apoptosis. Recently, we described the selection of SINE compound resistant cells and reported elevated expression of inflammation-related genes in these cells. Here, we demonstrated that NF-κB transcriptional activity is up-regulated in cells that are naturally resistant or have acquired resistance to SINE compounds. Resistance to SINE compounds was created by knockdown of the cellular NF-κB inhibitor, IκB-α. Combination treatment of selinexor with proteasome inhibitors decreased NF-κB activity, sensitized SINE compound resistant cells and showed synergistic cytotoxicity in vitro and in vivo. Furthermore, we showed that selinexor inhibited NF-κB activity by blocking phosphorylation of the IκB-α and the NF-κB p65 subunits, protecting IκB-α from proteasome degradation and trapping IκB-α in the nucleus to suppress NF-κB activity. Therefore, combination treatment of selinexor with a proteasome inhibitor may be beneficial to patients with resistance to either single-agent.
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Registered trials
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.