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Suppression of CaMKII? Inhibits ANO1-Mediated Glioblastoma Progression.


ABSTRACT: ANO1, a Ca2+-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 Ca2+/Calmodulin-dependent protein kinase II (CaMKII) ? 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 CaMKII?, among the four CaMKII isoforms, increased the surface expression and channel activity of ANO1 in a heterologous expression system. Additionally, gene silencing of CaMKII? suppressed the surface expression and channel activity of ANO1 in U251 cells. Moreover, gene silencing of CaMKII? or ANO1 prominently reduced the migration and invasion of U251 and U87 MG glioblastoma cells. We thus conclude that CaMKII? 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.

SUBMITTER: Sim KM 

PROVIDER: S-EPMC7290681 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Suppression of CaMKIIβ Inhibits ANO1-Mediated Glioblastoma Progression.

Sim Kyoung Mi KM   Lee Young-Sun YS   Kim Hee Jin HJ   Cho Chang-Hoon CH   Yi Gwan-Su GS   Park Myung-Jin MJ   Hwang Eun Mi EM   Park Jae-Yong JY  

Cells 20200426 5


ANO1, a Ca<sup>2+</sup>-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<sup>2+</sup>/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  ...[more]

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