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Interleukin-32 alpha induces migration of human melanoma cells through downregulation of E-cadherinopen access

Authors
Lee, JoohyunKim, Kyung EunCheon, SoyoungSong, Ju HanHouh, YounkyungKim, Tae SungGil, MinchanLee, Kyung JinKim, SeonghanKim, DaejinHur, Dae YoungYang, YoolheeBang, Sa IkPark, Hyun JeongCho, Daeho
Issue Date
Oct-2016
Publisher
Impact Journals
Keywords
interleukin-32; melanoma; migration; Erk1/2; E-cadherin
Citation
Oncotarget, v.7, no.40, pp 65825 - 65836
Pages
12
Journal Title
Oncotarget
Volume
7
Number
40
Start Page
65825
End Page
65836
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9393
DOI
10.18632/oncotarget.11669
ISSN
1949-2553
Abstract
Interleukin (IL)-32 alpha, the shortest isoform of proinflammatory cytokine IL32, is associated with various inflammatory diseases and cancers. However, its involvement in human melanoma is not understood. To determine the effect of IL-32 alpha in melanoma, IL-32 alpha levels were examined in human melanoma cell lines that exhibit different migratory abilities. IL-32 alpha levels were higher in human melanoma cell lines with more migratory ability. An IL-32 alpha-overexpressing G361 human melanoma cell line was generated to investigate the effect of IL-32 alpha on melanoma migration. IL-32 alpha-overexpressing G361 cells (G361-IL-32 alpha) exhibit an increased migratory ability compared to vector control cells (G361-vector). To identify factors involved in IL-32 alpha-induced migration, we compared expression of E-cadherin in G361-vector and G361-IL-32 alpha cells. We observed decreased levels of E-cadherin in G361-IL-32 alpha cells, resulting in F-actin polymerization. To further investigate signaling pathways related to IL-32 alpha-induced migration, we treated G361-vector and G361-IL-32 alpha cells with PD98059, a selective MEK inhibitor. Inhibition of Erk1/2 by PD98059 restored E-cadherin expression and decreased IL-32 alpha-induced migration. In addition, cell invasiveness of G361-IL-32 alpha cells was tested using an in vivo lung metastasis model. As results, lung metastasis was significantly increased by IL-32 alpha overexpression. Taken together, these data indicate that IL-32 alpha induced human melanoma migration via Erk1/2 activation, which repressed E-cadherin expression. Our findings suggest that IL-32 alpha is a novel regulator of migration in melanoma.
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대학 > 기초교양대학 > 기초교양학부 > 1. Journal Articles
원격대학원 > 향장미용전공 > 1. Journal Articles
원격대학원 > 향장미용학과 > 1. Journal Articles

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Kim, Kyung Eun
대학원 (헬스산업학(협동과정))
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