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Erianin as a Promising Novel Agent in the Treatment of Neuroblastoma: The Anticancer Effects and Underlying Molecular Mechanisms

[ Vol. 23 , Issue. 10 ]

Author(s):

Sema Serter Kocoglu*, Mücahit Seçme and Fatma Bahar Sunay   Pages 1204 - 1210 ( 7 )

Abstract:


<p>Background: Erianin is an active dibenzyl compound isolated from Dendrobium officinale and Dendrobium chrysotoxum and there are very few studies on molecular mechanisms and drug targets of erianin. In addition, there is no study investigating the anti-cancer effect of erianin on neuroblastoma cells. </p><p> Objective: The aim of the study is to investigate the anticancer effect of erianin and the underlying mechanism of this effect on SH-SY5Y cells. </p><p> Methods: The effects of erianin on cell viability, invasion and migration were determined by XTT, matrigel chamber and wound healing evaluation, respectively. Expression changes of miRNAs (microRNA) and apoptosis-related genes were evaluated by RT-PCR, and the apoptosis rate was supported by Annexin V evaluation. </p><p> Results: Erianin significantly decreased cell proliferation, invasion and migration. Erianin administration caused apoptosis by significantly increasing <i>caspase-7</i>, FADD (Fas-associated protein with death domain), <i>BID</i> (BH3 Interacting Domain Death Agonist) and <i>DR5</i> (Death receptor 5) gene expressions. While the rate of total apoptotic cells was 45.35 ± 6.80% in SH-SY5Y cells treated with erianin, it was 0.133 ± 0.05% in the control group (p = 0.000). In addition, erianin administration significantly decreased the expressions of hsa-miR-155-5p (p = 0.014) and hsa-miR-223-3p (p = 0.004). Also, our study demonstrated for the first time the relationship between erianin and mi-RNAs in a cancer cell. </p><p> Conclusion: Our study suggests that erianin may be a natural, safe and easily accessible drug candidate that can be used in the treatment of neuroblastoma.</p>

Keywords:

Neuroblastoma, erianin, apoptosis, miRNAs, anticancer, cell viability, invasion, migration.

Affiliation:

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