Histone Deacetylase Inhibitors Interact with Melanoma Differentiation Associated-7/Interleukin-24 to Kill Primary Human Glioblastoma Cells

Hamed, Hossein A.; Yacoub, Adly; Park, Margaret A.; Archer, Kellie J.; Das, Swadesh K.; Sarkar, Devanand; Grant, Steven; Fisher, Paul B.; Dent, Paul

doi:10.1124/mol.113.086553

Cited by 22 publications

(23 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Antibody reagents, other kinase inhibitors, caspase inhibitors cell culture reagents, and non-commercial recombinant adenoviruses have been previously described. [21][22][23][25][26][27][28] …”

Section: Methodsmentioning

confidence: 99%

HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells

Booth

Roberts

Conley

et al. 2013

Cancer Biology & Therapy

Self Cite

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells

Booth

Roberts

Conley

et al. 2013

Cancer Biology & Therapy

Self Cite

View full text Add to dashboard Cite

“…PERK inhibition blocked ceramide generation, which was critical for Ca 2+ elevation and subsequent ROS formation [ 136 ]. It was also demonstrated that histone deacetylase inhibitors enhance toxicity of IL-24 in invasive primary human GBM cells by synergizing with IL-24 killing effect [ 137 ]. Interestingly, enhanced lethality correlated with increased autophagy that was dependent on the expression of CerS6.…”

Section: Ceramide In Necrotic and Autophagic Death Of Gbm Cellsmentioning

confidence: 96%

The Role and Function of Sphingolipids in Glioblastoma Multiforme

Hadi

Vito

Marfia

et al. 2015

Bioactive Sphingolipids in Cancer Biology and Therapy

View full text Add to dashboard Cite

Aberrations in sphingolipid metabolism and thus levels have been implicated in promoting the aggressiveness of glioblastoma multiforme, one of the most lethal cancers in humans. A major player is sphingosine-1-phosphate, that pressures GBM cells to exhibit its hallmarks, leading to increased proliferation, invasiveness, stemness, angiogenesis and death resistance, this indicating a fi ne balance and interplay between S1P function and this malignancy. To the opposite GBM are organized to maintain low their ceramide and sphingomyelin levels, which in turn lead to a loss of growth control and to a gain of death resistance. While the mechanisms of these alterations are emerging, the sphingolipid signaling pathway has been implicated in controlling GBM action and mass, and in mediating the link of malignancy. Here we describe and discuss the current understanding on how GBM cells arm themselves with the abilities of manipulating sphingolipids, especially sphingosine-1-phosphate and ceramide, and how these alterations, through differential interactions, regulate different signaling

show abstract

“…It has also recently been shown that histone deacetylase inhibitors (HDACIs) increase MDA-7/IL-24 lethality through mechanisms involving ER stress and activation of the extrinsic apoptosis pathway (94). Adenoviral delivery of mda-7/IL-24 to GBM cells and tumors can be enhanced by a serotype 3 tropism modification and by engineering of the virus to conditionally replicate in tumor cells (99). This approach constitutes an attractive adjuvant therapeutic strategy for GBM.…”

Section: Gene Therapeutic Targets For Glioblastomamentioning

confidence: 99%

Adenoviral vector-mediated gene therapy for gliomas: coming of age

Castro

Candolfi

Wilson

et al. 2014

Expert Opinion on Biological Therapy

View full text Add to dashboard Cite

Introduction Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults; it carries a dismal prognosis. Adenoviral vector (Ad)-mediated gene transfer is being developed as a promising therapeutic strategy for GBM. Preclinical studies have demonstrated safety and efficacy of adenovirus administration into the brain and tumor mass in rodents and into the non-human primates’ brain. Importantly Ads have been safely administered within the tumor resection cavity in humans. Areas Covered Background on GBM and Ad vectors; we describe gene therapy strategies for GBM and discuss the value of combination approaches. Finally we discuss the results of the human clinical trials for GBM that have used adenoviral vectors. Expert Opinion The transduction characteristics of Ad vectors, and their safety profile, added to their capacity to achieve high levels of transgene expression have made them powerful vectors for the treatment of GBM. Recent gene therapy successes in the treatment of retinal diseases and systemic brain metabolic diseases, encourages the development of gene therapy for malignant glioma. Exciting clinical trials are currently recruiting patients; although it is large randomized phase III controlled clinical trials that will provide the final decision on the success of gene therapy for the treatment of GBM.

show abstract

Histone Deacetylase Inhibitors Interact with Melanoma Differentiation Associated-7/Interleukin-24 to Kill Primary Human Glioblastoma Cells

Cited by 22 publications

References 51 publications

HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells

HDAC inhibitors enhance the lethality of low dose salinomycin in parental and stem-like GBM cells

The Role and Function of Sphingolipids in Glioblastoma Multiforme

Adenoviral vector-mediated gene therapy for gliomas: coming of age

Contact Info

Product

Resources

About