Related Experiment Video

Updated: Apr 23, 2026

Reliably Engineering and Controlling Stable Optogenetic Gene Circuits in Mammalian Cells
09:20

Reliably Engineering and Controlling Stable Optogenetic Gene Circuits in Mammalian Cells

Published on: July 6, 2021

2.3K

Mitochondrial KATP Channels Control Glioma Radioresistance by Regulating ROS-Induced ERK Activation

Lianyan Huang1, Boxing Li, Shihao Tang

  • 1Department of Occupational Health and Occupational Medicine, School of Public Health and Tropical Medicine, Southern Medical University, 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.

Molecular Neurobiology
|September 25, 2014
PubMed

Insights

Mitochondrial ATP-sensitive potassium channels (mtK(ATP) channels) are overexpressed in glioma cells and drive radioresistance. Inhibiting these channels may improve glioma treatment by overcoming radioresistance.

Area of Science:

  • Neuro-oncology
  • Mitochondrial Biology
  • Cancer Therapeutics

Background:

  • Malignant glioma is a primary brain tumor with limited treatment options.
  • Glioma cell radioresistance significantly hinders radiotherapy efficacy.
  • Identifying novel targets to overcome radioresistance is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the role of mitochondrial ATP-sensitive potassium (mtK(ATP)) channels in glioma radioresistance.
  • To explore the relationship between mtK(ATP) channel expression, glioma malignancy, and patient survival.
  • To determine if mtK(ATP) channels regulate reactive oxygen species (ROS)-induced ERK activation in glioma.

Main Methods:

  • Quantitative analysis of mtK(ATP) channel expression in glioma tissues.
  • In vitro and in vivo experiments involving mtK(ATP) channel inhibition.
  • Assessment of reactive oxygen species (ROS) levels and ERK pathway activation.
  • Evaluation of glioma cell radiosensitivity following mtK(ATP) channel blockade.

Main Results:

  • mtK(ATP) channels are overexpressed in glioma and correlate with malignancy grade and reduced survival.
  • mtK(ATP) channels regulate glioma radioresistance via ROS-induced ERK activation.
  • Inhibition of mtK(ATP) channels significantly suppresses glioma radioresistance both in vitro and in vivo.
  • mtK(ATP) channel inhibition effectively reduces ERK activation.

Conclusions:

  • mtK(ATP) channels are key regulators of glioma radioresistance.
  • Targeting mtK(ATP) channels offers a promising strategy to enhance radiotherapy effectiveness.
  • mtK(ATP) channel blockers and MEK inhibitors represent potential therapeutic targets for glioma treatment.

More Related Videos

Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids10:26

Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids

Published on: October 21, 2022

2.3K

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
11.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.3K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.1K
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...
7.3K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.6K