Electrochemical Investigation of the Influence of K2[B3O3F4OH] on the Activity of Immobilized Superoxide Dismutase

Herenda, Safija; Ostojić, Jelena; Hasković, Edhem; Hasković, Denis; Galić, Borivoj

doi:10.20964/2018.04.35

Cited by 12 publications

(6 citation statements)

References 15 publications

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“…3A), the most prominent biological processes related to peptidase and endopeptidase activity implicate HB as possible peptidase regulator and protease binding moderator. This kind of HB activity might be expected because it was previously reported that HB interferes with different enzyme activities [41–44]. In addition, statistically significant inhibition of anti‐apoptotic BCL‐2 protein by HB 0.2 and 0.4 mg·mL −1 treatments was confirmed in UT‐7 leukemia only [17].…”

Section: Discussionmentioning

confidence: 64%

Halogenated boroxine increases propensity to apoptosis in leukemia (UT‐7) but not non‐tumor cells in vitro

et al. 2022

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A hallmark of the development of solid and hematological malignancies is the dysregulation of apoptosis, which leads to an imbalance between cell proliferation, cell survival and death. Halogenated boroxine [K2(B3O3F4OH)] (HB) is a derivative of cyclic anhydride of boronic acid, with reproducible anti‐tumor and anti‐proliferative effects in different cell models. Notably, these changes are observed to be more profound in tumor cells than in normal cells. Here, we investigated the underlying mechanisms through an extensive evaluation of (a) deregulated target genes and (b) their interactions and links with main apoptotic pathway genes upon treatment with an optimized concentration of HB. To provide deeper insights into the mechanism of action of HB, we performed identification, visualization, and pathway association of differentially expressed genes (DEGs) involved in regulation of apoptosis among tumor and non‐tumor cells upon HB treatment. We report that HB at a concentration of 0.2 mg·mL−1 drives tumor cells to apoptosis, whereas non‐tumor cells are not affected. Comparison of DEG profiles, gene interactions and pathway associations suggests that the HB effect and tumor‐‘selectivity’ can be explained by Bax/Bak‐independent mitochondrial depolarization by ROS generation and TRAIL‐like activation, followed by permanent inhibition of NFκB signaling pathway specifically in tumor cells.

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Section: Discussionmentioning

confidence: 64%

Halogenated boroxine increases propensity to apoptosis in leukemia (UT‐7) but not non‐tumor cells in vitro

et al. 2022

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“…We synthesised HB as a water-soluble white powder (99.99 % purity) at the University of Sarajevo, Faculty of Science, Laboratory for Physical Chemistry as described elsewhere (9)(10)(11)(12)(13)(14)(15)(16)(17)(18). HB stock solution was prepared by dissolving 20 mg of HB in 1 mL of the RPMI-1640 culture medium (Sigma-Aldrich, St. Louis, MO, USA).…”

Section: Halogenated Boroxine Synthesis and Solution Preparationmentioning

confidence: 99%

“…Previous studies of halogenated boroxine (HB) [K 2 (B 3 O 3 F 4 OH)] have shown promising therapeutic effects (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19), especially in view of the fact that cancer cells are more sensitive to HB than normal cells (11,12,19). Several studies reported that HB significantly affected the regulation of apoptosis-related genes in UT-7 human leukaemia (12,19).…”

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confidence: 99%

New in vitro findings about halogenated boroxine cytotoxicity and deregulation of cell death-related genes in GR-M melanoma cells

Elez-Burnjaković

Pojskić

Haverić

et al. 2023

Archives of Industrial Hygiene and Toxicology

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Anti-proliferative effects of halogenated boroxine – K2(B3O3F4OH) (HB) – have been confirmed in multiple cancer cell lines, including melanoma, but the exact mechanism of action is still unknown. This study aimed to determine its cytotoxic effects on human Caucasian melanoma (GR-M) cell growth in vitro as well as on the expression of cell death-related genes BCL-2, BECN1, DRAM1, and SQSTM1. GR-M and peripheral blood mononuclear (PBM) cells were treated with different HB concentrations and their growth inhibition and relative gene expression profiles were determined using the Alamar blue assay and real-time PCR. HB significantly inhibited cell growth of both GR-M and PBM cells but was even more effective in GR-M melanoma cells, as significant inhibition occurred at a lower HB concentration of 0.2 mg/mL. GR-M BCL-2 expression was significantly downregulated (P=0.001) at HB concentration of 0.4 mg/mL, which suggests that HB is a potent tumour growth inhibitor. At the same time, it upregulated BCL-2 expression in normal (PBM) cells, probably by activating protective mechanisms against induced cytotoxicity. In addition, all but the lowest HB concentrations significantly upregulated SQSTM1 (P=0.001) in GR-M cells. Upregulated BECN1 expression suggests early activation of autophagy at the lowest HB concentration in SQSTM1 cells and at all HB concentrations in PBM cells. Our findings clearly show HB-associated cell death and, along with previous cytotoxicity studies, reveal its promising anti-tumour potential.

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“…Patented as a prevention and therapeutic agent for various skin changes [ 19 , 20 ], HB has been submitted to numerous in vitro studies [ 21 , 22 , 23 , 24 , 25 ]. It acts as an inhibitor of horseradish peroxidase (HRP) [ 26 ], catalase [ 27 ], superoxide dismutase [ 28 ], and carbonic anhydrases [ 29 ]. In the GR-M cell line, HB significantly downregulates the relative expression of IGF-1 , hTERT , and BCL-2 genes [ 24 , 30 ], suggesting its antitumor activity.…”

Section: Introductionmentioning

confidence: 99%

Halogenated Boroxine K2[B3O3F4OH] Modulates Metabolic Phenotype and Autophagy in Human Bladder Carcinoma 5637 Cell Line

Elez-Burnjaković,

Pojskić,

Haverić

et al. 2024

Molecules

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Halogenated boroxine K2[B3O3F4OH] (HB), an inorganic derivative of cyclic anhydride of boronic acid, is patented as a boron-containing compound with potential for the treatment of both benign and malignant skin changes. HB has effectively inhibited the growth of several carcinoma cell lines. Because of the growing interest in autophagy induction as a therapeutic approach in bladder carcinoma (BC), we aimed to assess the effects of HB on metabolic phenotype and autophagy levels in 5637 human bladder carcinoma cells (BC). Cytotoxicity was evaluated using the alamar blue assay, and the degree of autophagy was determined microscopically. Mitochondrial respiration and glycolysis were measured simultaneously. The relative expression of autophagy-related genes BECN1, P62, BCL-2, and DRAM1 was determined by real-time PCR. HB affected cell growth, while starvation significantly increased the level of autophagy in the positive control compared to the basal level of autophagy in the untreated negative control. In HB-treated cultures, the degree of autophagy was higher compared to the basal level, and metabolic phenotypes were altered; both glycolysis and oxidative phosphorylation (OXPHOS) were decreased by HB at 0.2 and 0.4 mg/mL. Gene expression was deregulated towards autophagy induction and expansion. In conclusion, HB disrupted the bioenergetic metabolism and reduced the intracellular survival potential of BC cells. Further molecular studies are needed to confirm these findings and investigate their applicative potential.

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Electrochemical Investigation of the Influence of K2[B3O3F4OH] on the Activity of Immobilized Superoxide Dismutase

Cited by 12 publications

References 15 publications

Halogenated boroxine increases propensity to apoptosis in leukemia (UT‐7) but not non‐tumor cells in vitro

Halogenated boroxine increases propensity to apoptosis in leukemia (UT‐7) but not non‐tumor cells in vitro

New in vitro findings about halogenated boroxine cytotoxicity and deregulation of cell death-related genes in GR-M melanoma cells

Halogenated Boroxine K2[B3O3F4OH] Modulates Metabolic Phenotype and Autophagy in Human Bladder Carcinoma 5637 Cell Line

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