Cytotoxic activities and molecular mechanisms of the beauvericin and beauvericin G1 microbial products Against melanoma cells

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Title
Cytotoxic activities and molecular mechanisms of the beauvericin and beauvericin G1 microbial products Against melanoma cells
Author(s)
H N Lim; Jun-Pil Jang; H J Shin; Jae-Hyuk JangJong Seog Ahn; H J Jung
Bibliographic Citation
Molecules, vol. 25, no. 8, pp. 1974-1974
Publication Year
2020
Abstract
Melanoma is the most serious type of skin cancer and remains highly drug-resistant. Therefore, the discovery of novel effective agents against melanoma is in high demand. Herein, we investigated the cytotoxic activities in melanoma cells and underlying molecular mechanisms of beauvericin (BEA) and its analogue beauvericin G1 (BEA G1), which are cyclohexadepsipeptides isolated from fungi. BEA and BEA G1 significantly suppressed the growth, clonogenicity, migration, and invasion of A375SM human melanoma cells and promoted caspase-dependent apoptosis through upregulation of death receptors, as well as modulation of pro- and anti-apoptotic Bcl-2 family members. Furthermore, the effects of BEA and BEA G1 were associated with the suppression of multiple molecular targets that play crucial roles in melanoma oncogenesis, including ERK, JNK, p38, NF-κB, STAT3, and MITF. Notably, the cytotoxic efficacy of BEA G1 against A375SM cells was stronger than that of BEA. These findings suggest that BEA and BEA G1 can be further investigated as potent cytotoxic natural compounds for the suppression of melanoma progression. ⓒ 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Keyword
ApoptosisBeauvericinBeauvericin G1MelanomaMicrobial product
ISSN
1420-3049
Publisher
MDPI
DOI
http://dx.doi.org/10.3390/molecules25081974
Type
Article
Appears in Collections:
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
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