Time schedule-dependent effect of the CK2 inhibitor TBB on PC-3 human prostate cancer cell viability

Orzechowska, Emilia J.; Kozłowska, Ewa; Staroń, Krzysztof; Trzcińska-Danielewicz, Joanna

doi:10.3892/or.2011.1500

Cited by 5 publications

(5 citation statements)

References 38 publications

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“…For example, apigenin, TBCA, and CK2α or CK2α’ siRNA decrease nuclear translocation of AR (androgen-receptor) and AR-mediated gene expression in response to an AR agonist, R1881, treatment [ 146 ]. TBB sensitizes cells to TRAIL (tumor-necrosis factor-related ligand)/induced apoptosis and glycolysis inhibitors (2-DG) in PC-3 and ALVA-41 cells in a synergistic manner [ 150 , 151 ]. Conversely, overexpression of CK2α partially blocks TRAIL-induced apoptosis, caspase activity and caspase protein levels in ALVA-41 and PC-3 cells [ 152 ].…”

Section: Discussionmentioning

confidence: 99%

CK2 in Cancer: Cellular and Biochemical Mechanisms and Potential Therapeutic Target

et al. 2017

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CK2 genes are overexpressed in many human cancers, and most often overexpression is associated with worse prognosis. Site-specific expression in mice leads to cancer development (e.g., breast, lymphoma) indicating the oncogenic nature of CK2. CK2 is involved in many key aspects of cancer including inhibition of apoptosis, modulation of signaling pathways, DNA damage response, and cell cycle regulation. A number of CK2 inhibitors are now available and have been shown to have activity against various cancers in vitro and in pre-clinical models. Some of these inhibitors are now undergoing exploration in clinical trials as well. In this review, we will examine some of the major cancers in which CK2 inhibition has promise based on in vitro and pre-clinical studies, the proposed cellular and signaling mechanisms of anti-cancer activity by CK2 inhibitors, and the current or recent clinical trials using CK2 inhibitors.

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Section: Discussionmentioning

confidence: 99%

CK2 in Cancer: Cellular and Biochemical Mechanisms and Potential Therapeutic Target

et al. 2017

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“…Both fractions were resuspended in Annexin V binding buffer and pooled. Apoptotic cells were detected by flow cytometry as described previously [ 42 ] and analyzed with a BD FACSDiva Software ver. 6.0 (Becton Dickinson).…”

Section: Methodsmentioning

confidence: 99%

Controlled delivery of BID protein fused with TAT peptide sensitizes cancer cells to apoptosis

et al. 2014

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BackgroundLow cellular level of BID is critical for viability of numerous cancer cells. Sensitization of cells to anticancer agents by BID overexpression from adenovirus or pcDNA vectors is a proposed strategy for cancer therapy; however it does not provide any stringent control of cellular level of BID. The aim of this work was to examine whether a fusion of BID with TAT cell penetrating peptide (TAT-BID) may be used for controlled sensitization of cancer cells to anticancer agents acting through death receptors (TRAIL) or DNA damage (camptothecin). Prostate cancer PC3 and LNCaP, non-small human lung cancer A549, and cervix carcinoma HeLa cells were used in the study.MethodsUptake of TAT-BID protein by cells was studied by quantitative Western blot analysis of cells extracts. Cells viability was monitored by MTT test. Apoptosis was detected by flow cytometry and cytochrome c release assay.ResultsTAT-BID was delivered to all cancer cells in amounts depending on time, dose and the cell line. Recombinant BID sensitized PC3 cells to TRAIL or, to lesser extent, to camptothecin. Out of remaining cells, TAT-BID sensitized A549, and only slightly HeLa cells to TRAIL. None of the latter cell lines were sensitized to camptothecin. In all cases the mutant not phosphorylable by CK2 (TAT-BIDT59AS76A) was similarly efficient in sensitization as the wild type TAT-BID.ConclusionsTAT-BID may be delivered to cancer cells in controlled manner and efficiently sensitizes PC3 and A549 cells to TRAIL. Therefore, it may be considered as a potential therapeutic agent that enhances the efficacy of TRAIL for the treatment of prostate and non-small human lung cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2407-14-771) contains supplementary material, which is available to authorized users.

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“…In addition, the androgen-independent prostate cancer cell line PC-3 also displays relatively elevated CK2 activity compared to LNCaP prostate cells [19, 20]. In accordance with these observations, targeting CK2α with antisense RNA or inhibitors induces tumor shrinkage in a human prostate cancer xenograft model, suggesting the importance of CK2 in prostate tumorigenesis [3, 21, 22]. Although the importance of CK2 in tumor cell survival and growth is clear, the molecular mechanism by which CK2 is involved in prostate tumorigenesis has not been extensively investigated.…”

Section: Introductionmentioning

confidence: 79%

CK2-NCoR signaling cascade promotes prostate tumorigenesis

et al. 2013

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The aberrant expressions of casein kinase 2 (CK2) was found in prostate cancer patient and cell lines, but little is known of the detailed mechanisms implicated in prostate tumorigenesis. In this study, we report that both CK2 activity and CK2-mediated NCoR phosphorylation are significantly elevated in the androgen-independent prostate cancer cell line DU145 and PC-3 compared with RWPE1 and LNCaP cells. Increased phosphorylation inversely correlates with the mRNA level of the NCoR-regulated gene, interferon-γ-inducible protein 10 (IP-10). CK2 inhibition abrogated NCoR phosphorylation, IP-10 transcriptional repression, and the invasion activity of PC-3 cells. Inhibition of the CK2-NCoR network significantly reduced in vivo PC-3 cell tumorigenicity, likely due to transcriptional derepression of IP-10. Clinicopathological analyses revealed that increased CK2-mediated NCoR phosphorylation significantly correlates with poor survival among prostate cancer patients. These findings elucidate a CK2-modulated oncogenic cascade in prostate tumorigenesis.

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Time schedule-dependent effect of the CK2 inhibitor TBB on PC-3 human prostate cancer cell viability

Cited by 5 publications

References 38 publications

CK2 in Cancer: Cellular and Biochemical Mechanisms and Potential Therapeutic Target

CK2 in Cancer: Cellular and Biochemical Mechanisms and Potential Therapeutic Target

Controlled delivery of BID protein fused with TAT peptide sensitizes cancer cells to apoptosis

CK2-NCoR signaling cascade promotes prostate tumorigenesis

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