Related Experiment Video

Updated: Aug 21, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

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

Published on: April 13, 2015

[Telomerase SiRNA inhibits KB cell growth in human oral squamous cell carcinoma]

Zhi-qiang Yang1, Guang-sheng Chen, Jia-kun Chen

  • 1Department of Stomatology, The Second Affiliated Hospital, Guangzhou Medical College, Guangzhou 510260, China. Yangz@pub.guangzhou.gd.cn

Zhonghua Kou Qiang Yi Xue Za Zhi = Zhonghua Kouqiang Yixue Zazhi = Chinese Journal of Stomatology
|October 23, 2004
PubMed
Abstract

Insights

Small interfering RNA (siRNA) effectively reduced telomerase mRNA and suppressed oral squamous cell carcinoma KB cell growth by inhibiting cell cycle progression. This demonstrates siRNA

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Gene Silencing

Context:

  • Oral squamous cell carcinoma (OSCC) is a prevalent cancer globally.
  • Telomerase is a key enzyme in cancer cell immortalization and proliferation.
  • Targeting telomerase offers a potential therapeutic strategy for OSCC.

Purpose:

  • To evaluate the efficacy of small interfering RNA (siRNA) targeting telomerase mRNA in OSCC.
  • To assess the impact of telomerase inhibition on KB cell growth, cell cycle, and apoptosis.

Summary:

  • Synthesized 21-nucleotide siRNA duplexes targeting human telomerase mRNA.
  • Transfection of siRNA specifically suppressed telomerase mRNA and activity in KB cells for approximately 48 hours.
  • siRNA treatment reduced cell proliferation by 30% for 120 hours, primarily by blocking the G1 to S phase transition, without inducing apoptosis.

Impact:

  • siRNA demonstrates significant potential as a tool for functional genomics research.
  • siRNA holds promise as a gene-specific therapeutic agent for oral squamous cell carcinoma.

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

Related Concept Videos

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...
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.
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,...
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...
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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...