Inhibitory effects of selenium on telomerase activity and hTERT expression in cadmium-transformed 16HBE cells

Hua-Jie Chen1, Ri-An Yu, Ling-Fei He

  • 1Department of Occupational and Environmental Health, MOE Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.

Abstract

Insights

Sodium selenite inhibits telomerase activity in cadmium-transformed lung cells. This effect is linked to reduced hTERT and c-myc mRNA expression and increased mad1 mRNA expression, with a clear dose-response relationship.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Toxicology

Background:

  • Cadmium exposure can lead to cellular transformation and potentially cancer.
  • Telomerase is a key enzyme in cell immortalization and is often reactivated in cancer cells.
  • hTERT mRNA is a critical component for telomerase activity.

Purpose of the Study:

  • To investigate the impact of sodium selenite on telomerase activity.
  • To examine the effect of sodium selenite on human telomerase reverse transcriptase (hTERT) mRNA expression.
  • To analyze gene expression changes in cadmium-transformed 16HBE cells exposed to sodium selenite.

Main Methods:

  • Cadmium-transformed 16HBE cells were cultured and exposed to varying concentrations of sodium selenite (0.625-5.00 micromol/L) for 24 hours.
  • Telomerase activity was measured using standard assays.
  • Gene expression levels for hTERT, c-myc, mad1, hTRF1, and hTRF2 mRNA were quantified.

Main Results:

  • Sodium selenite significantly decreased telomerase activity in a dose-dependent manner.
  • Expression of hTERT and c-myc mRNA decreased, while mad1 mRNA expression increased following selenium exposure.
  • No significant changes were observed in hTRF1 and hTRF2 mRNA expression.

Conclusions:

  • Selenium effectively inhibits telomerase activity in cadmium-transformed 16HBE cells.
  • The inhibition mechanism involves down-regulation of hTERT and c-myc mRNA and up-regulation of mad1 mRNA.
  • A significant correlation exists between selenium concentration and these molecular changes.

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.
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...