Related Experiment Video

Updated: Jan 26, 2026

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays
07:42

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays

Published on: September 19, 2018

8.3K

Effects of Glycogen Synthase Kinase Inhibitor on Glioblastoma Multiforme Cell Line via Apoptosis and Cell Signaling

Mahmut Camlar1, Eda Acikgoz, Kenan Demir

  • 1University of Health Sciences, Tepecik Training and Research Hospital, Department of Neurosurgery, Izmir, Turkey.

Turkish Neurosurgery
|April 16, 2019
PubMed
Abstract

Insights

Glycogen synthase kinase-3 (GSK-3) inhibition shows promise for glioblastoma multiforme (GBM) treatment. Inhibiting GSK-3 induces GBM cell death and reduces key protein expression, offering a new therapeutic avenue.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Glioblastoma multiforme (GBM) is an aggressive brain tumor with limited treatment options.
  • Glycogen synthase kinase-3 (GSK-3) plays a role in cell proliferation and survival, making it a potential therapeutic target.

Purpose of the Study:

  • To investigate the effects of GSK-3 inhibition on apoptosis and molecular pathways in GBM.
  • To evaluate the impact of GSK-3 inhibition on Epidermal Growth Factor (EGF) and Nuclear Factor-kappa B (NF-kB) expression in GBM cells.

Main Methods:

  • Human GBM (U-87 MG) and glial (SVGp12) cell lines were treated with a GSK-3 inhibitor.
  • Apoptosis was assessed using DNA fragmentation (TUNEL assay).
  • EGFR and NF-kB expression levels were measured via immunofluorescence.

Main Results:

  • GSK-3 inhibitor IX induced dose-dependent cytotoxicity and apoptosis in GBM cells.
  • Inhibition of GSK-3 led to a significant decrease in both NF-kB and EGFR expression.
  • The GSK-3 inhibitor demonstrated effectiveness in reducing GBM cell proliferation.

Conclusions:

  • GSK-3 inhibition is a promising strategy for GBM therapeutic management.
  • Modulating EGFR and NF-kB expression are key mechanisms through which GSK-3 inhibition induces apoptosis in GBM.
  • Targeting GSK-3 offers potential for novel GBM treatment approaches.

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

9.5K
Author Spotlight: Innovative Cancer Therapies with Iron Oxide Nanoparticles for Glioblastoma Treatment09:02

Author Spotlight: Innovative Cancer Therapies with Iron Oxide Nanoparticles for Glioblastoma Treatment

Published on: September 27, 2024

3.1K

Related Concept Videos

Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
Protein kinases
Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
15.0K
What is Cell Signaling?02:03

What is Cell Signaling?

Despite the protective membrane that separates a cell from the environment, cells need the ability to detect and respond to environmental changes. Additionally, cells often need to communicate with one another. Unicellular and multicellular organisms use a variety of cell signaling mechanisms to communicate to respond to the environment.
130.0K
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,...
8.4K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.3K
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
6.5K
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
9.9K