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. 2024 Nov 12;22:541. doi: 10.1186/s12964-024-01913-2

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Bromoxib exhibits cytotoxic effects in various cancer cell lines and triggers apoptosis through the intrinsic mitochondria-dependent pathway. Cytotoxicity was determined after 24 h with increasing concentrations of bromoxib in various human cancer cell lines: (A) Leukemia and lymphoma cell lines: HL60 (acute myeloid leukemia; AML), HPBALL (T cell acute lymphoblastic leukemia; T-ALL), Jurkat (T-ALL), KOPTK (T-ALL), MOLT4 (T-ALL), SUPB15 (B cell acute lymphoblastic leukemia; B-ALL), K652 (chronic myeloid leukemia; CML), Ramos (Burkitt B cell lymphoma), and (B) solid tumor cell lines: HeLa (cervical cancer), MCF7 (breast cancer), RT112 (bladder cancer), LN209, LN308, YKG1, SJ-GBM2, and TP365MG (different glioblastoma cell lines). Cell viability was assessed by AlamarBlue^® viability assay. Shown in each graph is the mean ± SD of one representative experiment performed in triplicates. The respective IC₅₀ values are shown within the graphs. n.d.=not determinable in the depicted concentration range. (C) Bromoxib induces caspase 8 independent and (D) caspase 9 dependent apoptosis. After incubating for 24 h, apoptosis-related DNA degradation was observed by measuring propidium iodide-stained apoptotic hypodiploid nuclei using flow cytometry in (C) caspase 8-positive and caspase 8-negative Jurkat cells and (D) caspase 9-positive and caspase 9-negative Jurkat cells. Cells were stimulated with bromoxib (10 µM), staurosporine (STS; 2.5 µM), etoposide (Etopo; 50 µM), and DMSO (0.1% v/v; diluent control). For stimulation of death receptors in (C) TRAIL (Tumor Necrosis Factor Related Apoptosis Inducing Ligand; 40 ng/ml) or (D) CD95-ligand (CD95L) (500 ng/ml) were applied. Error bars = mean ± SD of three independent experiments performed in triplicates. (E) Bromoxib-induced apoptosis is blocked in the presence of antiapoptotic Bcl-2. Apoptosis induction was analyzed in Jurkat cells stably transfected with vectors encoding Bcl-2 or empty vector. After 24 h apoptosis induction was assessed by propidium iodide staining of apoptotic nuclei and flow-cytometry. Cells were treated with different concentrations of bromoxib (left panel) and respective controls, STS (2.5 µM), Etopo (50 µM), and DMSO (0.1% v/v) (right panel). Error bars = mean ± SD of three independent experiments performed in triplicates