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Updated: Mar 2, 2026

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

Published on: April 13, 2015

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Targeting human telomerase RNA component using antisense oligonucleotide induces rapid cell death and increases

Leila Asghari-Kia1, Davood Bashash1, Ava Safaroghli-Azar1

  • 1Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

European Journal of Pharmacology
|May 24, 2017
PubMed

Insights

Targeting telomerase with hTR ASODN induces apoptosis in cancer cells. Combining this telomerase inhibitor with arsenic trioxide (ATO) enhances cell death, offering a promising strategy for acute promyelocytic leukemia (APL) treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Telomerase inhibition is a promising cancer therapy strategy.
  • Telomerase plays a role in cancer cell survival and proliferation.
  • Arsenic trioxide (ATO) is used in treating acute promyelocytic leukemia (APL).

Purpose of the Study:

  • To investigate the efficacy of targeting human telomerase RNA template (hTR) using an oligonucleotide-based molecule (hTR ASODN) in cancer cells.
  • To evaluate the synergistic effect of hTR ASODN in combination with ATO.
  • To elucidate the molecular mechanisms underlying the combined treatment's effects.

Main Methods:

  • Treatment of NB4 cells with hTR ASODN as a single agent and in combination with ATO.
  • Assessment of cell survival rates and apoptosis.
  • Analysis of DNA damage response pathways, including p73, ATM, c-Myc, and p21 expression.

Main Results:

  • hTR ASODN reduced NB4 cell survival and induced caspase-3-dependent apoptosis.
  • Combination therapy with ATO and hTR ASODN showed enhanced reduction in cell viability.
  • The combined treatment activated DNA damage response via p73 and ATM upregulation, and c-Myc downregulation.
  • Induction of p21 and altered death promoter/repressor gene balance contributed to growth suppression.

Conclusions:

  • Telomerase activity can attenuate ATO effectiveness in APL treatment.
  • Combining ATO with a telomerase inhibitor like hTR ASODN is a novel and promising strategy.
  • This combination therapy may improve cure rates for APL.
Keywords:
APLApoptosisArsenic trioxideTelomerase

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