ArticleJournal of cancer research and clinical oncology2012
Histone deacetylase inhibitor potentiates chemotherapy-induced apoptosis through Bim upregulation in Burkitt's lymphoma cells.
Article in Journal of cancer research and clinical oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting RAD51-BRCA2 Interaction to Enhance Synthetic Lethality with Olaparib in Pancreatic Cancer: Development of a Novel Phenyl Furan-Quinoline-Carboxylic Acid Series.ACS medicinal chemistry letters · 2026Article
- GANT-61 Induces Autophagy and Apoptosis in Glioblastoma Cells despite their heterogeneity.Cellular and molecular neurobiology · 2021Article
- Current understanding of the role and regulation of miRNAs in Burkitt lymphoma.Blood and lymphatic cancer : targets and therapy · 2018Review
- Histone acetyltransferases and histone deacetylases in B- and T-cell development, physiology and malignancy.Genes & cancer · 2015Review
- Autophagy interplays with apoptosis and cell cycle regulation in the growth inhibiting effect of Trisenox in HEP-2, a laryngeal squamous cancer.Pathology oncology research : POR · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAlthough polychemotherapy regiments have improved clinical outcome for Burkitt's lymphoma (BL) patients, salvage treatment of patients with refractory disease remains very poor. Combined therapies protocols have been emerging to improve treatment strategies to circumvent responseless BL patients. We evaluate the cell death effect of histone deacetylase inhibitor (HDACI) combined with etoposide (VP-16) and cisplatin (CDDP) on BL cell lines.
methods3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay was performed to assess drug toxicity. To establish the concentrations and time of incubation for the combined treatment, a kinetic analysis was performed for each drug on BL41 and Raji BL cell lines for 24, 48 and 72 h. Apoptosis was assessed by flow cytometry using Annexin V/propidium iodide (PI) and cleaved caspase 3 labeling assays. Caspase 9 activation and levels of Bcl-2 family proteins were analyzed by Western blot.
resultsThe doses of NaB (1.0 mM), CDDP (1.0 and 2.5 μM), and VP-16 (0.1 and 0.3 μM) after 24 h of incubation were chosen for the evaluation of combined therapy. The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P < 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P < 0.05). However, Bim overexpression was not correlated with Bcl-2 inhibition (P > 0.05) and was accompanied by increase in Bax expression (P < 0.05). The combination effects of NaB/VP-16 and NaB/CDDP were found to be synergistic and additive, respectively, in both the cell lines.
conclusionsThe study provides strong evidence for the synergistic effects of the association with HDCI and chemotherapy in BL cells.
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