Related Experiment Video

Updated: Aug 14, 2026

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
12:08

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

Exogenous expression of p16INK4a is associated with decrease in telomerase activity

H Sawa1, H Kamada, T A Ohshima

  • 1Department of Neurosurgery, Kyorin University, School of Medicine, Mitaka, Tokyo, Japan.

Journal of Neuro-Oncology
|June 9, 1999
PubMed

Insights

Exogenous p16INK4a expression suppressed glioblastoma cell growth and altered cell morphology. This study reveals p16INK4a

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioblastoma is an aggressive brain tumor with limited treatment options.
  • Understanding the molecular mechanisms regulating glioblastoma cell proliferation is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the effect of exogenous p16INK4a expression on the biological characteristics of glioblastoma cells.
  • To determine if p16INK4a can modulate glioblastoma cell growth, cell cycle, and telomerase activity.

Main Methods:

  • Gene transfection of human glioblastoma U87MG cells with pVgRXR and pIND plasmids containing the wild-type p16 gene.
  • Regulation of p16INK4a expression using the ecdysone analogue, muristerone A.
  • Assessment of cell growth, morphology, cell cycle progression (Ki-67), and telomerase activity.

Main Results:

  • Exogenous p16INK4a expression reduced glioblastoma cell growth capacity.
  • Observed morphological changes included increased cell size and flattening.
  • p16INK4a expression inhibited cell cycle entry and decreased telomerase activity.

Conclusions:

  • Exogenous p16INK4a expression has a significant inhibitory effect on glioblastoma cell biological characteristics.
  • p16INK4a acts as a suppressor of glioblastoma cell proliferation and may be a potential therapeutic target.

More Related Videos

Telomerase Activity in the Various Regions of Mouse Brain: Non-Radioactive Telomerase Repeat Amplification Protocol (TRAP) Assay10:14

Telomerase Activity in the Various Regions of Mouse Brain: Non-Radioactive Telomerase Repeat Amplification Protocol (TRAP) Assay

Published on: September 2, 2014

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Related Concept Videos

Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
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...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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,...