Histone deacetylase inhibition induces apoptosis and autophagy in human neuroblastoma cells

Francisco, Roser; Pérez-Perarnau, Alba; Cortés, Constanza; Gil, Joan; Tauler, Albert; Ambrosio, Santiago

doi:10.1016/j.canlet.2011.11.036

Cited by 30 publications

(32 citation statements)

References 43 publications

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“…Moreover, these effects of butyrate and TSA on VSMC are consistent with their effects on other cell types. While butyrate arrests cell proliferation and stimulate morphological changes of variety of cell types, and in certain cell types the changes mirror the normal phenotype [13], TSA inhibits proliferation and causes cytotoxicity and apoptosis [27,28,29,30]. …”

Section: Resultsmentioning

confidence: 99%

“…However, butyrate has been shown to arrest proliferation of a wide range of cells and exhibit atypical effects on G1-specifc cyclin D1 and D3 in a cell type specific manner [34,35,36,37,38]. On the other hand, TSA, which has been shown to arrest proliferation and/or stimulate apoptosis of a variety of cells, causes downregulation of cyclin D1 [27,28,29,39,40,41], although in some cases TSA also increased cyclin D3 similar to butyrate [35]. Even though very limited information is available regarding the effects of butyrate [17,42] and TSA [3,25] on VSMC, particularly on D-type cyclins, upregulation of both cyclin D1 and D3 observed in VSMC in response to butyrate treatment appears to be unique to VSMC but significance of it is not clear.…”

Section: Resultsmentioning

confidence: 99%

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Differential Cellular and Molecular Effects of Butyrate and Trichostatin A on Vascular Smooth Muscle Cells

et al. 2012

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The histone deacetylase (HDAC) inhibitors, butyrate and trichostatin A (TSA), are epigenetic histone modifiers and proliferation inhibitors by downregulating cyclin D1, a positive cell cycle regulator, and upregulating p21Cip1 and INK family of proteins, negative cell cycle regulators. Our recent study indicated cyclin D1 upregulation in vascular smooth muscle cells (VSMC) that are proliferation-arrested by butyrate. Here we investigate whether cyclin D1 upregulation is a unique response of VSMC to butyrate or a general response to HDAC inhibitors (HDACi) by evaluating the effects of butyrate and TSA on VSMC. While butyrate and TSA inhibit VSMC proliferation via cytostatic and cytotoxic effects, respectively, they downregulate cdk4, cdk6, and cdk2, and upregulate cyclin D3, p21Cip1 and p15INK4B, and cause similar effects on key histone H3 posttranslational modifications. Conversely, cyclin D1 is upregulated by butyrate and inhibited by TSA. Assessment of glycogen synthase 3-dependent phosphorylation, subcellular localization and transcription of cyclin D1 indicates that differential effects of butyrate and TSA on cyclin D1 levels are linked to disparity in cyclin D1 gene expression. Disparity in butyrate- and TSA-induced cyclin D1 may influence transcriptional regulation of genes that are associated with changes in cellular morphology/cellular effects that these HDACi confer on VSMC, as a transcriptional modulator.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Differential Cellular and Molecular Effects of Butyrate and Trichostatin A on Vascular Smooth Muscle Cells

et al. 2012

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“…In fact, several reports has been shown that SAHA and other HDAC-inhibitors enhances tumor cell apoptosis through induction of proapoptotic proteins, such as Bim, Noxa and PUMA. 37, 38 Therefore, it could not denied the possibility that induction of apoptosis, but not suppression of cancer stem cell, by HDAC inhibitor is mainly involved in these effects.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin-enriching cancer stem cells confer multidrug resistance in non-small cell lung cancer via enhancing TRIB1/HDAC activity

et al. 2017

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Chemotherapeutic agents are generally used as a frontline therapy for non-small cell lung cancer (NSCLC). However, resistance to chemotherapy arises rapidly in NSCLC, and the reasons for chemotherapy resistance have not been fully determined. Here, we found cisplatin, but not paclitaxel and doxorubicin, induced the enrichment of cancer stem cell (CSC) and conferred multidrug resistance in NSCLC cell lines. In vivo study confirmed drug-resistant tumors displayed the enhanced expressions of CSC transcription factors. Mechanistically, cisplatin treatment resulted in C/EBP-β-dependent increasing of TRIB1. The crucial role of TRIB1 in cisplatin-induced enrichment of CSC and drug resistance was verified by knockdown TRIB1. Interestingly, cisplatin treatment also contributed to the increasement of HDAC, the interaction of TRIB1 with HDAC, and inactivation of p53. Similarly, the silencing of HDAC led to reduction of cisplatin-induced CSC, and combined knockdown of HDAC and TRIB1 exhibited enhanced effect. Additionally, the combination of HDAC inhibitor and cisplatin showed a reinforced antitumor action in NSCLC cell lines with TRIB1-dependent manner and remarkably shrink tumors in xenograft models. Moreover, cisplatin-treated NSCLC patients with high levels of TRIB1 exhibited a significantly poorer prognosis. Our findings illustrate a novel perspective in the evolution of chemotherapy resistance and provide a promising approach for the treatment of patients with NSCLC.

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“…The genesis of cancer, malignant dissemination of tumor cells are, at least in part, based on the up-regulation of histone deacetylases (HDACs). So HDACIs are emerging as promising clinical therapeutics for cancer (Bellarosa et al, 2012;Feng et al, 2012;Francisco et al, 2012).…”

Section: Effects Of Valproic Acid On Proliferation Apoptosis Angiogmentioning

confidence: 99%

Effects of Valproic Acid on Proliferation, Apoptosis, Angiogenesis and Metastasis of Ovarian Cancer in Vitro and in Vivo

Song¹,

Rong²,

Geng³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Inhibitors of histone deacetylase activity are emerging as a potentially important new class of anticancer agents. In this study, we assessed the anticancer effects of valproic acid (VPA) on ovarian cancer in vitro and in vivo. Cultured SKOV3 cells were treated by VPA with different concentrations and time, then the effects on cell growth, cell cycle, apoptosis, and related events were investigated. A human ovarian cancer model transplanted subcutaneously in nude mice was established, and the efficacy of VPA used alone and in combination with diammine dichloroplatinum (DDP) to inhibit the growth of tumors was also assessed. Proliferation of SKOV3 cells was inhibited by VPA in a dose and time dependent fashion. The cell cycle distribution changed one treatment with VPA, with decrease in the number of S-phase cells and increase in G1-phase. VPA could significantly inhibit the growth of the epithelial ovarian cancer SKOV3 cells in vivo without toxic side effects. Treatment with VPA combined with DDP demonstrated enhanced anticancer effects. The result of flow cytometry (FCM) indicated that after VPA in vitro and in vivo, the expression of E-cadherin was increased whereas vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) were decreased. This study suggests that VPA could be a novel attractive agent for treatment of ovarian cancer.

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Histone deacetylase inhibition induces apoptosis and autophagy in human neuroblastoma cells

Cited by 30 publications

References 43 publications

Differential Cellular and Molecular Effects of Butyrate and Trichostatin A on Vascular Smooth Muscle Cells

Differential Cellular and Molecular Effects of Butyrate and Trichostatin A on Vascular Smooth Muscle Cells

Cisplatin-enriching cancer stem cells confer multidrug resistance in non-small cell lung cancer via enhancing TRIB1/HDAC activity

Effects of Valproic Acid on Proliferation, Apoptosis, Angiogenesis and Metastasis of Ovarian Cancer in Vitro and in Vivo

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