ArticleMolecular oncology2012
Blockade of NFκB activity by Sunitinib increases cell death in Bortezomib-treated endometrial carcinoma cells.
Article in Molecular oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Sensitizing endometrial cancer to ionizing radiation by multi-tyrosine kinase inhibition.Journal of gynecologic oncology · 2020Article
- From Seabed to Bedside: A Review on Promising Marine Anticancer Compounds.Biomolecules · 2020Review
- Precision medicine by designer interference peptides: applications in oncology and molecular therapeutics.Oncogene · 2020Review
- SQSTM1/p62 loss reverses the inhibitory effect of sunitinib on autophagy independent of AMPK signaling.Scientific reports · 2019Article
- The effects of bortezomib on the ovariectomy applied rat uterus: A histopathological, stereological, and immunohistochemical study.Iranian journal of basic medical sciences · 2018Article
- Aurantoside C Targets and Induces Apoptosis in Triple Negative Breast Cancer Cells.Marine drugs · 2018Article
- Autophagy Inhibition Enhances Sunitinib Efficacy in Clear Cell Ovarian Carcinoma.Molecular cancer research : MCR · 2017Article
- Sunitinib depletes myeloid-derived suppressor cells and synergizes with a cancer vaccine to enhance antigen-specific immune responses and tumor eradication.Oncoimmunology · 2015Article
- Molecular profiling of circulating tumor cells links plasticity to the metastatic process in endometrial cancer.Molecular cancer · 2014Article
- Prognostic biomarkers in endometrial and ovarian carcinoma.Virchows Archiv : an international journal of pathology · 2014Review
- Article
- A phase 1 Bayesian dose selection study of bortezomib and sunitinib in patients with refractory solid tumor malignancies.British journal of cancer · 2013Article
- Blockade of NFκB activity by Sunitinib increases cell death in Bortezomib-treated endometrial carcinoma cells.Molecular oncology · 2012Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial carcinoma is one of the most common malignancies in the female genital tract, usually treated by surgery and radiotherapy. Chemotherapy is used when endometrial carcinoma is associated with widespread metastasis or when the tumor recurs after radiation therapy. In the present study, we demonstrate that the tyrosine kinase receptor inhibitor Sunitinib reduces cell viability, proliferation, clonogenicity and induces apoptotic cell death in endometrial carcinoma cell lines, which is not due to its action through the most known targets like VEGFR, nor through EGFR as demonstrated in this work. Interestingly, Sunitinib reduces NFκB transcriptional activity either at basal level or activation by EGF or TNF-α. We observed that Sunitinib was able to inhibit the Bortezomib-induced NFκB transcriptional activity which correlates with a decrease of the phosphorylated levels of IKKα and β, p65 and IκBα. We evaluated the nature of the interaction between Sunitinib and Bortezomib by the dose effect method and identified a synergistic effect (combination index < 1). Analogously, silencing of p65 expression by lentiviral-mediated short-hairpin RNA delivery in Bortezomib treated cells leads to a strongly increased sensitivity to Bortezomib apoptotic cell death. Altogether our results suggest that the combination of Sunitinib and Bortezomib could be considered a promising treatment for endometrial carcinoma after failure of surgery and radiation.
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