Comparative evaluation of the treatment efficacy of suberoylanilide hydroxamic acid (SAHA) and paclitaxel in ovarian cancer cell lines and primary ovarian cancer cells from patients

Sonnemann, Jürgen; Gänge, Jennifer; Pilz, S; Stötzer, Christine; Öhlinger, R.; Belau, A.; Lorenz, Gerd; Beck, James F.

doi:10.1186/1471-2407-6-183

Cited by 54 publications

(34 citation statements)

References 34 publications

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“…Notably, suberoylanilide hydroxamic acid (SAHA) has been demonstrated to act on VCR-resistant leukaemia cell lines (Ruefli et al, 2002), adriamycinresistant breast (Castro-Galache et al, 2003) and paclitaxel-resistant ovarian cancer cells (Sonnemann et al, 2006). SAHA at 5mM significantly diminished UKF-NB-3 CDDP or UKF-NB-3 VCR proliferation and cell adhesion to HUVEC in our own experiments (data not shown).…”

Section: Discussionmentioning

confidence: 64%

“…Most notably, recent data indicate that HDAC inhibition may be successful in treating refractory or relapsing tumours after conventional chemotherapy. Histone deacetylase inhibition has been demonstrated to block cell growth of drug-resistant small-cell lung cancer lines (Tsurutani et al, 2003), abrogate resistance in breast cancer cells (Hirokawa et al, 2005) and induce apoptosis in drug-resistant ovarian cancer cells (Sonnemann et al, 2006), myeloma cells (Maiso et al, 2006) and hepatoma cell lines (Pathil et al, 2006).…”

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confidence: 99%

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Valproic acid inhibits adhesion of vincristine- and cisplatin-resistant neuroblastoma tumour cells to endothelium

et al. 2007

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Drug resistance to chemotherapy is often associated with increased malignancy in neuroblastoma (NB). In pursuit of alternative treatments for chemoresistant tumour cells, we tested the response of multidrug-resistant SKNSH and of vincristine (VCR)-, doxorubicin (DOX)-, or cisplatin (CDDP)-resistant UKF-NB-2, UKF-NB-3 or UKF-NB-6 NB tumour cell lines to valproic acid (VPA), a differentiation inducer currently in clinical trials. Drug resistance caused elevated NB adhesion (UKF-NB-2 VCR , UKF-NB-2 DOX , UKF-NB-2 CDDP , UKF-NB-3 VCR , UKF-NB-3 CDDP , UKF-NB-6 VCR , UKF-NB-6 CDDP ) to an endothelial cell monolayer, accompanied by downregulation of the adhesion receptor neural cell adhesion molecule (NCAM). Based on the UKF-NB-3 model, N-myc proteins were enhanced in UKF-NB-3 VCR and UKF-NB-3 CDDP , compared to the drug naïve controls. p73 was diminished, whereas the p73 isoform deltaNp73 was upregulated in UKF-NB-3 VCR and UKF-NB-3 CDDP . Valproic acid blocked adhesion of UKF-NB-3 VCR and UKF-NB-3 CDDP , but not of UKF-NB-3 DOX , and induced the upregulation of NCAM surface expression, NCAM protein content and NCAM coding mRNA. Valproic acid diminished N-myc and enhanced p73 protein level, coupled with downregulation of deltaNp73 in UKF-NB-3 VCR and UKF-NB-3 CDDP . Valproic acid also reverted enhanced adhesion properties of drug-resistant UKF-NB-2, UKF-NB-6 and SKNSH cells, and therefore may provide an alternative approach to the treatment of drug-resistant NB by blocking invasive processes.

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Section: Discussionmentioning

confidence: 64%

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confidence: 99%

Valproic acid inhibits adhesion of vincristine- and cisplatin-resistant neuroblastoma tumour cells to endothelium

et al. 2007

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“…Toxicities were cancer cell lines treated with vorinostat demonstrated an accumulation of cells in G1 and G2, induced apoptosis, and increased levels of acetylated histones 3 and 4 [9]. In addition, HDAC inhibitors combined with chemotherapy such as platinum agents and paclitaxel resulted in synergy [10][11][12][13]. Increased platinum adduct formation of the open DNA configuration facilitated by HDAC inhibition has been proposed as a potential mechanism of action for increased cisplatin-induced cell kill [12,14].…”

Section: Introductionmentioning

confidence: 99%

Phase I study of combination of vorinostat, carboplatin, and gemcitabine in women with recurrent, platinum-sensitive epithelial ovarian, fallopian tube, or peritoneal cancer

Matulonis

Berlin

Lee

et al. 2015

Cancer Chemother Pharmacol

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“…We investigated whether HDIs belonging to two different structural classes, the hydroxamic acid derivative suberoylanilide hydroxamic acid (SAHA; vorinostat) and the short-chain fatty acid sodium butyrate (NaB), and aspirin interacted synergistically to induce cell death in an ovarian cancer cell line. Ovarian cancer appeared to be particularly interesting, because i) treatment with NSAIDs including aspirin have been demonstrated in vitro to reduce tumor growth (10), ii) an ovarian cancer mouse model study suggests that addition of SAHA could potentially increase the efficacy of the standard chemotherapeutic agent paclitaxel (11), and iii) in a recent ex vivo study we showed that SAHA had efficient activity against patient-derived ovarian cancer cells, which displayed only marginal responsiveness to paclitaxel (12). In this study, we show that the combination of HDIs with aspirin produced synergistic cytotoxic effects in A2780 ovarian cancer cells, while the combination of HDIs with selective COX inhibitors had no effect.…”

Section: Introductionmentioning

confidence: 99%

Histone deacetylase inhibitors and aspirin interact synergistically to induce cell death in ovarian cancer cells

Sonnemann

Hüls²,

Sigler³

et al. 2008

Oncol Rep

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Abstract. Histone deacetylase inhibitors (HDIs) as well as non-steroidal anti-inflammatory drugs including aspirin show promise as antineoplastic agents. The treatment with both HDIs and aspirin can result in hyperacetylation of proteins. In this study, we investigated whether HDIs and aspirin interacted in inducing anticancer activity and histone acetylation. We found that the HDIs, suberoylanilide hydroxamic acid and sodium butyrate, and aspirin cooperated to induce cell death in the ovarian cancer cell line, A2780. The effect was synergistic, as evidenced by CI-isobologram analysis. However, aspirin had no effect on histone acetylation, neither in the absence nor presence of HDIs. To gain insight into the mechanism underlying the synergistic action of HDIs and aspirin, we employed the deacetylated metabolite of aspirin, salicylic acid, and the cyclooxygenase-1-and -2-selective inhibitors, SC-560 and NS-398, respectively. We found that HDIs and salicylic acid interacted synergistically, albeit less efficiently than HDIs and aspirin, to induce cancer cell death, suggesting that the acetyl and the salicyl moiety contributed to the cooperative interaction of aspirin with HDIs. SC-560 and NS-398 had little effect both when applied alone or in conjunction with HDIs, indicating that the combinatorial effect of HDIs and aspirin was not the result of cyclo-oxygenase inhibition. In conclusion, our study demonstrates that HDIs and aspirin synergize to induce cancer cell death and, thus, provides a rationale for a more in-depth exploration into the potential of combining HDIs and aspirin as a strategy for anticancer therapy.

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Comparative evaluation of the treatment efficacy of suberoylanilide hydroxamic acid (SAHA) and paclitaxel in ovarian cancer cell lines and primary ovarian cancer cells from patients

Cited by 54 publications

References 34 publications

Valproic acid inhibits adhesion of vincristine- and cisplatin-resistant neuroblastoma tumour cells to endothelium

Valproic acid inhibits adhesion of vincristine- and cisplatin-resistant neuroblastoma tumour cells to endothelium

Phase I study of combination of vorinostat, carboplatin, and gemcitabine in women with recurrent, platinum-sensitive epithelial ovarian, fallopian tube, or peritoneal cancer

Histone deacetylase inhibitors and aspirin interact synergistically to induce cell death in ovarian cancer cells

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