Related Experiment Video

Updated: Dec 22, 2025

The In ovo CAM-assay as a Xenograft Model for Sarcoma
12:44

The In ovo CAM-assay as a Xenograft Model for Sarcoma

Published on: July 17, 2013

26.1K

Suppression of CaMKIIβ Inhibits ANO1-Mediated Glioblastoma Progression

Kyoung Mi Sim1, Young-Sun Lee1,2, Hee Jin Kim1,3

  • 1School of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul 02841, Korea.

Cells
|May 3, 2020
PubMed

Insights

Calcium/calmodulin-dependent protein kinase II beta (CaMKIIβ) specifically boosts ANO1 surface expression and activity in glioblastoma cells. This enhances glioblastoma cell migration and invasion, highlighting CaMKIIβ as a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • ANO1 (Anc1/TMEM16A) is a calcium-activated chloride channel highly expressed in glioblastoma.
  • ANO1 surface expression is implicated in glioblastoma cell migration and invasion.
  • Mechanisms regulating ANO1 surface expression in glioblastoma remain largely uncharacterized.

Purpose of the Study:

  • To investigate the role of calcium/calmodulin-dependent protein kinase II (CaMKII) in regulating ANO1 surface expression and activity in glioblastoma cells.
  • To determine the specific CaMKII isoform responsible for ANO1 regulation.
  • To elucidate the impact of CaMKII-mediated ANO1 regulation on glioblastoma cell migration and invasion.

Main Methods:

  • Utilized U251 and U87 MG glioblastoma cell lines.
  • Employed CaMKII inhibition using KN-93.
  • Performed gene silencing of CaMKIIβ and ANO1.
  • Assessed ANO1 surface expression and channel activity.
  • Evaluated cell migration and invasion assays.

Main Results:

  • CaMKIIβ specifically enhances ANO1 surface expression and channel activity in U251 glioblastoma cells.
  • Inhibition of CaMKII by KN-93 significantly reduces ANO1 surface expression and activity.
  • Gene silencing of CaMKIIβ suppresses ANO1 surface expression and activity.
  • CaMKIIβ and ANO1 are crucial for glioblastoma cell migration and invasion.

Conclusions:

  • CaMKIIβ plays a specific role in upregulating ANO1 surface expression and activity in glioblastoma.
  • CaMKIIβ-ANO1 axis contributes significantly to glioblastoma cell migration and invasion.
  • Targeting CaMKIIβ may represent a novel therapeutic strategy for glioblastoma.
Keywords:
ANO1CaMKIIβU251 glioblastoma cellsU87 MG glioblastoma cells

More Related Videos

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells12:52

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

16.3K
Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion09:23

Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion

Published on: October 20, 2016

14.6K

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
7.1K
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
6.5K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.6K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
8.0K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.7K