ArticleMolecular cancer therapeutics2008
Differential bortezomib sensitivity in head and neck cancer lines corresponds to proteasome, nuclear factor-kappaB and activator protein-1 related mechanisms.
Article in Molecular cancer therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Trial
- ER stress affects proliferation and induces polyploidization of cultured human HaCaT and A431 cells.Histochemistry and cell biology · 2026Article
- Inhibition of USP14 promotes TNFα-induced cell death in head and neck squamous cell carcinoma (HNSCC).Cell death and differentiation · 2023Article
- Review on Bortezomib Resistance in Multiple Myeloma and Potential Role of Emerging Technologies.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Proteasome inhibition by bortezomib parallels a reduction in head and neck cancer cells growth, and an increase in tumor-infiltrating immune cells.Scientific reports · 2021Article
- Apoptosis signaling molecules as treatment targets in head and neck squamous cell carcinoma.The Laryngoscope · 2020Article
- Regulation of NFκB Signalling by Ubiquitination: A Potential Therapeutic Target in Head and Neck Squamous Cell Carcinoma?Cancers · 2020Review
- Human Papillomavirus Infection in Head and Neck Squamous Cell Carcinomas: Transcriptional Triggers and Changed Disease Patterns.Frontiers in cellular and infection microbiology · 2020Review
- In HPV-Positive HNSCC Cells, Functional Restoration of the p53/p21 Pathway by Proteasome Inhibitor Bortezomib Does Not Affect Radio- or Chemosensitivity.Translational oncology · 2019Article
- The regulation of combined treatment-induced cell death with recombinant TRAIL and bortezomib through TRAIL signaling in TRAIL-resistant cells.BMC cancer · 2018Article
- CCR 20th anniversary commentary: Preclinical study of proteasome inhibitor bortezomib in head and neck cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- COMMD1/Murr1 reinforces HIV-1 latent infection through IκB-α stabilization.Journal of virology · 2015Article
- MEK inhibitor PD-0325901 overcomes resistance to CK2 inhibitor CX-4945 and exhibits anti-tumor activity in head and neck cancer.International journal of biological sciences · 2015Article
- Article
- HSP90 Inhibitor SNX5422/2112 Targets the Dysregulated Signal and Transcription Factor Network and Malignant Phenotype of Head and Neck Squamous Cell Carcinoma.Translational oncology · 2013Article
- Expression of vascular endothelial growth factor and transcription factors HIF-1, NF-kB expression in squamous cell carcinoma of head and neck; association with proteasome and calpain activities.Journal of cancer research and clinical oncology · 2013Article
- Inhibitory kappa B Kinases as targets for pharmacological regulation.British journal of pharmacology · 2012Review
- The 26S proteasome complex: an attractive target for cancer therapy.Biochimica et biophysica acta · 2012Review
- Early tumor progression associated with enhanced EGFR signaling with bortezomib, cetuximab, and radiotherapy for head and neck cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Catechol polymers for pH-responsive, targeted drug delivery to cancer cells.Journal of the American Chemical Society · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Head and neck squamous cell carcinomas (HNSCC) exhibit constitutive activation of transcription factors nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), which are modulated by the proteasome and promote resistance to cell death. HNSCC show variable sensitivity to the proteasome inhibitor bortezomib in vitro as well as in murine xenografts and patient tumors in vivo, and the mechanisms are not well understood. To address this question, the sensitivities of nine HNSCC cell lines to bortezomib were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, and the potential relationship between the sensitivity and bortezomib effects on biological processes was examined in HNSCC lines of differential bortezomib sensitivity. The most sensitive cell line (UM-SCC-11B) underwent cell death at 10(-9) mol/L in vitro and tumor regression at a maximally tolerated dose of bortezomib in a murine xenograft model. The differential sensitivity between UM-SCC-11A and UM-SCC-11B cells corresponded to differences in the extent of suppression of proteasome activity, ubiquitinated protein degradation, and NF-kappaB and AP-1 activation. Lower concentrations of bortezomib transiently increased NF-kappaB and sustained AP-1 activation in UM-SCC-11A cells. AP-1 reporter activity and cell density of UM-SCC-11A were suppressed when bortezomib was combined with c-Jun NH(2)-terminal kinase and p38 kinase pathways inhibitors. Thus, the differential sensitivities to bortezomib corresponded to dissimilar effects on the proteasome, NF-kappaB and AP-1 activities. Inhibition of c-Jun NH(2)-terminal kinase and p38 pathways blocked AP-1 activity and enhanced the antitumor effects. These findings revealed molecular mechanisms of bortezomib sensitivity and resistance, which are under development as biomarkers for clinical trials in patients with HNSCC.
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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.