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Suppression of CaMKIIÎ2 Inhibits ANO1-Mediated Glioblastoma Progression by Sim, Kyoung Mi; Lee, Young-Sun; Kim, Hee Jin; Cho, Chang-Hoon; Yi, Gwan-Su; Park, Myung-Jin; Hwang, Eun Mi; Park, Jae-Yong is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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ANO1, a Ca^2+^-activated chloride channel, is highly expressed in glioblastoma cells and its surface expression is involved in their migration and invasion. However, the regulation of ANO1 surface expression in glioblastoma cells is largely unknown. In this study, we found that Ca^2+^/Calmodulin-dependent protein kinase II (CaMKII) β specifically enhances the surface expression and channel activity of ANO1 in U251 glioblastoma cells. When KN-93, a CaMKII inhibitor, was used to treat U251 cells, the surface expression and channel activity of ANO1 were significantly reduced. Only CaMKIIβ, among the four CaMKII isoforms, increased the surface expression and channel activity of ANO1 in a heterologous expression system. Additionally, gene silencing of CaMKIIβ suppressed the surface expression and channel activity of ANO1 in U251 cells. Moreover, gene silencing of CaMKIIβ or ANO1 prominently reduced the migration and invasion of U251 and U87 MG glioblastoma cells. We thus conclude that CaMKIIβ plays a specific role in the surface expression of ANO1 and in the ANO1-mediated tumorigenic properties of glioblastoma cells, such as migration and invasion.

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Author

Sim, Kyoung Mi; Lee, Young-Sun; Kim, Hee Jin; Cho, Chang-Hoon; Yi, Gwan-Su; Park, Myung-Jin; Hwang, Eun Mi; Park, Jae-Yong

Publisher

Multidisciplinary Digital Publishing Institute (MDPI) (ISSN 2073-4409)

Published

2020

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)