Related Experiment Video

Updated: Jul 18, 2026

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction
08:41

Caspase-3 Activity in the Rat Amygdala Measured by Spectrofluorometry After Myocardial Infarction

Published on: January 12, 2016

hTERT/re-caspase-3 system induce apoptosis in hTERT-positive cancer cells

Li-fang Yang1, Yan Zhao, Liang Zeng

  • 1Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha, China.

Cancer Biology & Therapy
|December 19, 2006
PubMed

Insights

This study developed a cancer treatment using the human telomerase reverse transcriptase (hTERT) promoter to deliver a gene that induces apoptosis. This targeted approach effectively killed cancer cells and suppressed tumor growth in mice.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Apoptosis induction is a key strategy for cancer treatment.
  • Targeting cancer-specific mechanisms like telomerase offers a promising therapeutic avenue.
  • Human telomerase reverse transcriptase (hTERT) is highly active in most cancers but not normal cells.

Purpose of the Study:

  • To develop a telomerase-specific gene delivery system for inducing apoptosis in cancer cells.
  • To evaluate the antitumor efficacy of the hTERT-driven re-Caspase-3 gene therapy system.

Main Methods:

  • Utilized the hTERT promoter to drive expression of the apoptosis-inducing gene re-Caspase-3.
  • Tested the system's efficacy in hTERT-positive cancer cell lines (CNE1, HRT-18, MGC) and hTERT-low normal cells (Hacat).
  • Assessed the antitumor effect by observing tumor growth suppression in nude mice bearing subcutaneous tumors.

Main Results:

  • The hTERT/re-Caspase-3 system successfully induced apoptosis in hTERT-positive cancer cells.
  • No significant apoptosis was observed in hTERT-low normal cells, indicating specificity.
  • Significant suppression of subcutaneous tumor growth was achieved in treated nude mice.

Conclusions:

  • The hTERT promoter-driven re-Caspase-3 gene delivery system demonstrates cancer-specific apoptosis induction.
  • This telomerase-targeted gene therapy approach shows significant potential for effective cancer treatment.
  • The re-Caspase-3 gene's autocatalytic properties enhance its apoptosis-inducing capability.

More Related Videos

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Analysis of Apoptosis in Zebrafish Embryos by Whole-mount Immunofluorescence to Detect Activated Caspase 308:20

Analysis of Apoptosis in Zebrafish Embryos by Whole-mount Immunofluorescence to Detect Activated Caspase 3

Published on: December 20, 2013

Related Concept Videos

Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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...