Class I-specific histone deacetylase inhibitor MS-275 overrides TRAIL-resistance in melanoma cells by downregulating c-FLIP

Venza, Isabella; Visalli, Maria; Oteri, Rosaria; Teti, Diana

doi:10.1016/j.intimp.2014.05.024

Cited by 41 publications

(36 citation statements)

References 37 publications

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“…Depsipeptide is another member of HDACi that leads to caspase-dependent apoptosis in chronic lymphocytic leukemia and osteosarcoma cells through selectively involving TNF-R (extrinsic pathway) and down-regulation of c-FLIP without evidence of Fas (CD95) up-regulation (Aron et al, 2003;Watanabe et al, 2005). Additionally, MS-275 has been reported to block c-FLIP expression in CLL, osteosarcoma and melanoma cells (Lucas et al, 2004;Rao-Bindal et al, 2013;Venza et al, 2014). Recently, a small molecule inhibitor of c-FLIP, 4-(4-Chloro-2-methylphenoxy)-N-hydroxybutanamide (CMH), has been recognized as using a high-throughput chemical library screen (Schimmer et al, 2006).…”

Section: Targeting C-flipmentioning

confidence: 99%

Molecular Mechanisms of Apoptosis and Roles in Cancer Development and Treatment

Goldar¹,

Khaniani²,

Derakhshan³

et al. 2015

Asian Pacific Journal of Cancer Prevention

459

317

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Programmed cell death (PCD) or apoptosis is a mechanism which is crucial for all multicellular organisms to control cell proliferation and maintain tissue homeostasis as well as eliminate harmful or unnecessary cells from an organism. Defects in the physiological mechanisms of apoptosis may contribute to different human diseases like cancer. Identification of the mechanisms of apoptosis and its effector proteins as well as the genes responsible for apoptosis has provided a new opportunity to discover and develop novel agents that can increase the sensitivity of cancer cells to undergo apoptosis or reset their apoptotic threshold. These novel targeted therapies include those targeting anti-apoptotic Bcl-2 family members, p53, the extrinsic pathway, FLICE-inhibitory protein (c-FLIP), inhibitor of apoptosis (IAP) proteins, and the caspases. In recent years a number of these novel agents have been assessed in preclinical and clinical trials. In this review, we introduce some of the key regulatory molecules that control the apoptotic pathways, extrinsic and intrinsic death receptors, discuss how defects in apoptotic pathways contribute to cancer, and list several agents being developed to target apoptosis.

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Section: Targeting C-flipmentioning

confidence: 99%

Molecular Mechanisms of Apoptosis and Roles in Cancer Development and Treatment

Goldar¹,

Khaniani²,

Derakhshan³

et al. 2015

Asian Pacific Journal of Cancer Prevention

459

317

View full text Add to dashboard Cite

show abstract

“…5A). Absence or downregulation of caspase 8 is a frequent event in cancer correlated with unfavorable outcome (Pingoud-Meier et al, 2003;Yang et al, 2007), which may cause resistance to apoptosis (Venza et al, 2014;Van Geelen et al, 2010). Several studies have demonstrated that expression of caspase 8 may be controlled by epigenetic modifications which differ according to the type of cancer cells Kikuchi et al, 2013;Lin et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…qPCR was performed by ABI Prism 7500 real-time PCR System (Applied Biosystems, Milan, Italy). Primers and probes were previously reported (Venza et al, 2014;Kanao et al, 2004;Venza et al, 2013;Goyal et al, 2008). The mRNA levels of p14 ARF , p16 INK4A , caspase 8, death receptor 4 (DR4), death receptor 5 (DR5), E-cadherin (CDH1), DNMT1, DNMT3a, and DNMT3b were normalized to endogenous b-actin (Applied Biosystems).…”

Section: Reverse Transcription and Quantitative Real-time Pcr (Qpcr)mentioning

confidence: 99%

“…As in melanoma p14 ARF , p16 INK4A , and CDH1 silencing contributes to progression, metastasis, and cell proliferation (Law et al, 2012;Lobos-González et al, 2013) and a crucial role has been given to the extrinsic pathway of apoptosis (Venza et al, 2014), to dissect the molecular mechanism of Cd action on melanoma cell growth, we have examined whether the expression of p14 ARF , p16 INK4A , E-cadherin, caspase 8, DR4, and DR5 has been affected by Cd exposure. Fig.…”

Section: Effect Of CD On the Expression Of Tumor-related Genesmentioning

confidence: 99%

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Epigenetic marks responsible for cadmium-induced melanoma cell overgrowth

Venza

Visalli

Biondo

et al. 2015

Toxicology in Vitro

Self Cite

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“…The usefulness of such cooperation between TRAIL and HDACIs in treating melanoma was shown in different studies. Melanoma cells were induced to apoptosis when TRAIL was applied together with a HDACI known as SBHA, while other research points to a higher apoptosis rate due to the interactive effects of applying TRAIL together with the inhibitors known as MS-275 and MC1575 [170,171].…”

Section: Epigenetic Treatmentmentioning

confidence: 99%

New Frontiers in Melanoma Epigenetics—The More We Know, the More We Don’t Know

Nguyen

Dobosz

2017

Epigenomes

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Skin cancer is one of the most common neoplasms worldwide, with a surprising tendency to increase its incidence. As with many cancer types nowadays, early diagnosis and proper management carries an excellent prognosis, up to 5-year survival rate of above 95% for most skin cancers, even though the long-term survival rate among metastatic melanoma patients remains only 5%. This review aims to summarize recent discoveries in epigenetic changes connected with cutaneous malignant melanoma (CMM), comprising of DNA methylation, histone modifications, miRNA regulation, nucleosome positioning and chromatin remodelling. Undoubtedly, personalised medicine based on both genetic and epigenetic changes of cancer is the future, the question remains: how long will it take to transport this treatment from the bench to the bedside?

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Class I-specific histone deacetylase inhibitor MS-275 overrides TRAIL-resistance in melanoma cells by downregulating c-FLIP

Cited by 41 publications

References 37 publications

Molecular Mechanisms of Apoptosis and Roles in Cancer Development and Treatment

Molecular Mechanisms of Apoptosis and Roles in Cancer Development and Treatment

Epigenetic marks responsible for cadmium-induced melanoma cell overgrowth

New Frontiers in Melanoma Epigenetics—The More We Know, the More We Don’t Know

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