Cell Survival Signaling in Neuroblastoma

Megison, Michael L.; Gillory, Lauren A.; Beierle, Elizabeth A.

doi:10.2174/1871520611313040005

Cited by 34 publications

(35 citation statements)

References 134 publications

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“…Another protein firmly involved in angiogenesis of neuroblastoma is vascular endothelial growth factor (VEGF) (5,6). As expected, one of the control levels is transcription-related to the interaction between IL-8 and VEGF promoters and different transcription factors, such as NF-κB, AP-1 and C-EBP/NF-IL-6 (7)(8)(9)(10)(11)(12). In addition, the expression of IL-8 and VEGF genes may be under the control of epigenetic mechanisms, such as those regulated by microRNAs in cancer, differentiation and inflammatory processes (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 68%

MicroRNA miR-93-5p regulates expression of IL-8 and VEGF in neuroblastoma SK-N-AS cells

et al. 2016

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Abstract. The role of the microRNA miR-93-5p on the secretome profile and the expression levels of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) was investigated in the neuroblastoma SK-N-AS cell line by Bio-Plex analysis and RT-qPCR. The results indicate that VEGF and IL-8 are the major miR-93-5p molecular targets. This conclusion was based on in vitro transfection with pre-miR-93-5p and anti-miR-93-5p; these treatments inversely modulated both VEGF and IL-8 gene expression and protein release in the neuroblastoma SK-N-AS cell line. Computational analysis showed the presence of miR-93-5p consensus sequences in the 3'UTR region of both VEGF and IL-8 mRNAs, predicting possible interaction with miR-93-5p and confirming a potential regulatory role of this microRNA.

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Section: Introductionmentioning

confidence: 68%

MicroRNA miR-93-5p regulates expression of IL-8 and VEGF in neuroblastoma SK-N-AS cells

et al. 2016

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“…Our study was focused on the genes identified as prognosis markers and potential therapeutic targets of neuroblastoma [4, 5, 21, 23, 24]. Concerning poor prognosis factors, when gene expression was modulated by both citalopram and escitalopram, the action was always a decrease except for MDM2 and VEGFA .…”

Section: Discussionmentioning

confidence: 99%

“…Genetic analysis of tumor samples performed in the last two decades correlated these prognostic disparities to an extensive series of genetic features actually considered as the prognosis markers of the disease notably MYCN [4, 5]. Those associated with a poor clinical outcome have become the potential targets for the development of new therapeutic approaches.…”

Section: Introductionmentioning

confidence: 99%

Assessment of citalopram and escitalopram on neuroblastoma cell lines: Cell toxicity and gene modulation

Sakka

Delétage²,

Chalus

et al. 2017

Oncotarget

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Selective serotonin reuptake inhibitors (SSRI) are common antidepressants which cytotoxicity has been assessed in cancers notably colorectal carcinomas and glioma cell lines. We assessed and compared the cytotoxicity of 2 SSRI, citalopram and escitalopram, on neuroblastoma cell lines. The study was performed on 2 non-MYCN amplified cell lines (rat B104 and human SH-SY5Y) and 2 human MYCN amplified cell lines (IMR32 and Kelly). Citalopram and escitalopram showed concentration-dependent cytotoxicity on all cell lines. Citalopram was more cytotoxic than escitalopram. IMR32 was the most sensitive cell line. The absence of toxicity on human primary Schwann cells demonstrated the safety of both molecules for myelin. The mechanisms of cytotoxicity were explored using gene-expression profiles and quantitative real-time PCR (qPCR). Citalopram modulated 1 502 genes and escitalopram 1 164 genes with a fold change ≥ 2. 1 021 genes were modulated by both citalopram and escitalopram; 481 genes were regulated only by citalopram while 143 genes were regulated only by escitalopram. Citalopram modulated 69 pathways (KEGG) and escitalopram 42. Ten pathways were differently modulated by citalopram and escitalopram. Citalopram drastically decreased the expression of MYBL2, BIRC5 and BARD1 poor prognosis factors of neuroblastoma with fold-changes of -107 (p<2.26 10−7), -24.1 (p<5.6 10−9) and -17.7 (p<1.2 10−7). CCNE1, AURKA, IGF2, MYCN and ERBB2 were more moderately down-regulated by both molecules. Glioma markers E2F1, DAPK1 and CCND1 were down-regulated. Citalopram displayed more powerful action with broader and distinct spectrum of action than escitalopram.

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“…1 Unfortunately, 5-year overall survival rates are still only around 60% for RA-treated patients. [7][8][9] Frequently, overactivation of survival pathways prevents cell-cycle arrest or apoptosis in neuroblastoma cells (reviewed by Megison et al 10 ). [7][8][9] Frequently, overactivation of survival pathways prevents cell-cycle arrest or apoptosis in neuroblastoma cells (reviewed by Megison et al 10 ).…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid–induced survival effects in SH‐SY5Y neuroblastoma cells

Waetzig

Haeusgen

Andres

et al. 2018

J of Cellular Biochemistry

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Neuroblastoma is a malignant childhood cancer arising from the embryonic sympathoadrenal lineage of the neural crest. Retinoic acid (RA) is included in the multimodal therapy of patients with high‐risk neuroblastoma to eliminate minimal residual disease. However, the formation of RA‐resistant cells substantially lowers 5‐year overall survival rates. To examine mechanisms that lead to treatment failure, we chose human SH‐SY5Y cells, which are known to tolerate incubation with RA by activating the survival kinases Akt and extracellular signal‐regulated kinase 1/2. Characterization of downstream pathways showed that both kinases increased the phosphorylation of the ubiquitin ligase mouse double minute homolog 2 (Mdm2) and thereby enhanced p53 degradation. When p53 signaling was sustained by blocking complex formation with Mdm2 or enhancing c‐Jun N‐terminal kinase (JNK) activation, cell viability was significantly reduced. In addition, Akt‐mediated phosphorylation of the cell‐cycle regulator p21 stimulated complex formation with caspase‐3, which also contributed to cell protection. Thus, treatment with RA augmented survival signaling and attenuated basal apoptotic pathways in SH‐SY5Y cells, which increased cell viability.

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Cell Survival Signaling in Neuroblastoma

Cited by 34 publications

References 134 publications

MicroRNA miR-93-5p regulates expression of IL-8 and VEGF in neuroblastoma SK-N-AS cells

MicroRNA miR-93-5p regulates expression of IL-8 and VEGF in neuroblastoma SK-N-AS cells

Assessment of citalopram and escitalopram on neuroblastoma cell lines: Cell toxicity and gene modulation

Retinoic acid–induced survival effects in SH‐SY5Y neuroblastoma cells

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