Sodium valproate potentiates staurosporine‐induced apoptosis in neuroblastoma cells via Akt/survivin independently of HDAC inhibition

Shah, Reecha D.; Jagtap, Jayashree C.; Mruthyunjaya, S.; Shelke, Ganesh Vilas; Pujari, Radha; Das, Gowry; Shastry, Padma

doi:10.1002/jcb.24422

Cited by 17 publications

(16 citation statements)

References 37 publications

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“…This kind of approach has already been used with other HDACis to demonstrate the specificity of the anti-HDAC activity effect (20)(21)(22). Interestingly, both derivatives did not have any effect on cell growth or on CSC population ( Supplementary Fig.…”

Section: Histone Deacetylase Inhibitors Modulate Breast Cancer Stem Cmentioning

confidence: 93%

The Histone Deacetylase Inhibitor Abexinostat Induces Cancer Stem Cells Differentiation in Breast Cancer with Low Xist Expression

Salvador

Wicinski

Cabaud

et al. 2013

Clinical Cancer Research

119

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Purpose: Cancer stem cells (CSC) are the tumorigenic cell population that has been shown to sustain tumor growth and to resist conventional therapies. The purpose of this study was to evaluate the potential of histone deacetylase inhibitors (HDACi) as anti-CSC therapies.Experimental Design: We evaluated the effect of the HDACi compound abexinostat on CSCs from 16 breast cancer cell lines (BCL) using ALDEFLUOR assay and tumorsphere formation. We performed gene expression profiling to identify biomarkers predicting drug response to abexinostat. Then, we used patientderived xenograft (PDX) to confirm, in vivo, abexinostat treatment effect on breast CSCs according to the identified biomarkers.Results: We identified two drug-response profiles to abexinostat in BCLs. Abexinostat induced CSC differentiation in low-dose sensitive BCLs, whereas it did not have any effect on the CSC population from high-dose sensitive BCLs. Using gene expression profiling, we identified the long noncoding RNA Xist (Xinactive specific transcript) as a biomarker predicting BCL response to HDACi. We validated that low Xist expression predicts drug response in PDXs associated with a significant reduction of the breast CSC population.Conclusions: Our study opens promising perspectives for the use of HDACi as a differentiation therapy targeting the breast CSCs and identified a biomarker to select patients with breast cancer susceptible to responding to this treatment.

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Section: Histone Deacetylase Inhibitors Modulate Breast Cancer Stem Cmentioning

confidence: 93%

The Histone Deacetylase Inhibitor Abexinostat Induces Cancer Stem Cells Differentiation in Breast Cancer with Low Xist Expression

Salvador

Wicinski

Cabaud

et al. 2013

Clinical Cancer Research

119

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“…Kramer and colleagues suggested that induction of cancer cell apoptosis with the treatment of HDACi such as VPA is driven by hyperacetylation of Stat1 that allow its interaction with NF-kB and reduces NF-kB signaling [191], thus suppressing expression of NF-kB target genes including Bcl-XL, survivin, and Stat5. A study shows that valpromide (VPM), an amide analog of VPA that does not inhibit HDAC also potentiates cell death in cancer cells associated with decreased level of survivin indicating an alternative mechanism of VPA-mediated apoptosis [192]. Farnesylthiosalicylic acid, a Ras inhibitor was tested in combination with VPA.…”

Section: Therapeutic Targeting Of Survivinmentioning

confidence: 99%

Survivin, a molecular target for therapeutic interventions in squamous cell carcinoma

Khan

Yadav

et al. 2017

Cell Mol Biol Lett

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Squamous cell carcinoma (SCC) is the most common cancer worldwide. The treatment of locally advanced disease generally requires various combinations of radiotherapy, surgery, and systemic therapy. Despite aggressive multimodal treatment, most of the patients relapse. Identification of molecules that sustain cancer cell growth and survival has made molecular targeting a feasible therapeutic strategy. Survivin is a member of the Inhibitor of Apoptosis Protein (IAP) family, which is overexpressed in most of the malignancies including SCC and totally absent in most of the normal tissues. This feature makes survivin an ideal target for cancer therapy. It orchestrates several important mechanisms to support cancer cell survival including inhibition of apoptosis and regulation of cell division. Overexpression of survivin in tumors is also associated with poor prognosis, aggressive tumor behavior, resistance to therapy, and high tumor recurrence. Various strategies have been developed to target survivin expression in cancer cells, and their effects on apoptosis induction and tumor growth attenuation have been demonstrated. In this review, we discuss recent advances in therapeutic potential of survivin in cancer treatment.

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“…Multiple mechanisms have been proposed to explain the potent anticancer activity of HDAC inhibitors in neuroblastoma cells. For example, the effect of a HDAC inhibitor VPA on apoptosis was mediated by repression of survivin and Akt pathway [23]. In addition to histones, HDACs also target numerous non-histone proteins such as Ku70, p53 and HSP90 [24].…”

Section: Introductionmentioning

confidence: 99%

RuvBL2 Is Involved in Histone Deacetylase Inhibitor PCI-24781-Induced Cell Death in SK-N-DZ Neuroblastoma Cells

Zhan

Tsai

et al. 2013

PLoS ONE

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Neuroblastoma is the second most common solid tumor diagnosed during infancy. The survival rate among children with high-risk neuroblastoma is less than 40%, highlighting the urgent needs for new treatment strategies. PCI-24781 is a novel hydroxamic acid-based histone deacetylase (HDAC) inhibitor that has high efficacy and safety for cancer treatment. However, the underlying mechanisms of PCI-24781 are not clearly elucidated in neuroblastoma cells. In the present study, we demonstrated that PCI-24781 treatment significantly inhibited tumor growth at very low doses in neuroblastoma cells SK-N-DZ, not in normal cell line HS-68. However, PCI-24781 caused the accumulation of acetylated histone H3 both in SK-N-DZ and HS-68 cell line. Treatment of SK-N-DZ with PCI-24781 also induced cell cycle arrest in G2/M phase and activated apoptosis signaling pathways via the up-regulation of DR4, p21, p53 and caspase 3. Further proteomic analysis revealed differential protein expression profiles between non-treated and PCI-24781 treated SK-N-DZ cells. Totally 42 differentially expressed proteins were identified by MALDI-TOF MS system. Western blotting confirmed the expression level of five candidate proteins including prohibitin, hHR23a, RuvBL2, TRAP1 and PDCD6IP. Selective knockdown of RuvBL2 rescued cells from PCI-24781-induced cell death, implying that RuvBL2 might play an important role in anti-tumor activity of PCI-24781 in SK-N-DZ cells. The present results provide a new insight into the potential mechanism of PCI-24781 in SK-N-DZ cell line.

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Sodium valproate potentiates staurosporine‐induced apoptosis in neuroblastoma cells via Akt/survivin independently of HDAC inhibition

Cited by 17 publications

References 37 publications

The Histone Deacetylase Inhibitor Abexinostat Induces Cancer Stem Cells Differentiation in Breast Cancer with Low Xist Expression

The Histone Deacetylase Inhibitor Abexinostat Induces Cancer Stem Cells Differentiation in Breast Cancer with Low Xist Expression

Survivin, a molecular target for therapeutic interventions in squamous cell carcinoma

RuvBL2 Is Involved in Histone Deacetylase Inhibitor PCI-24781-Induced Cell Death in SK-N-DZ Neuroblastoma Cells

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