Related Experiment Video

Updated: Aug 25, 2026

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
08:51

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

Published on: June 25, 2015

IRF-1-mediated CAS expression enhances interferon-gamma-induced apoptosis of HT-29 colon adenocarcinoma cells

M C Jiang1, T L Lin, T L Lee

  • 1Institute of Zoology, Academia Sinica, Taipei 11529, Taiwan, Republic of China.

Molecular Cell Biology Research Communications : MCBRC
|November 13, 2001
PubMed

Insights

Cancer susceptibility protein (CAS) enhances tumor cell apoptosis. Interferon-gamma (IFN-gamma) induces CAS expression, increasing cell death and suggesting CAS as a potential cancer elimination target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cancer susceptibility protein (CAS) expression is upregulated in human tumors and linked to tumor development.
  • CAS plays a role in apoptosis, the process of programmed cell death.
  • Understanding CAS's role in apoptosis is crucial for developing cancer therapies.

Purpose of the Study:

  • To investigate if CAS expression influences the susceptibility of tumor cells to IFN-gamma-induced apoptosis.
  • To elucidate the role of Interferon-gamma (IFN-gamma) and IRF-1 in regulating CAS expression in tumor cells.

Main Methods:

  • HT-29 tumor cells were treated with IFN-gamma.
  • CAS expression levels were analyzed following IFN-gamma treatment.
  • IRF-1's role in mediating IFN-gamma-induced CAS expression was investigated.
  • Apoptosis and CPP32 expression were assessed in cells with varying CAS expression levels.

Main Results:

  • IFN-gamma treatment induced CAS expression in HT-29 cells, mediated by the transcriptional factor IRF-1.
  • While CAS overexpression alone did not induce apoptosis, it significantly enhanced IFN-gamma-induced apoptosis.
  • CAS overexpression also enhanced IFN-gamma-induced CPP32 expression, a key apoptosis executioner molecule.

Conclusions:

  • Tumor cells with high CAS expression are more susceptible to apoptosis induced by agents that upregulate CAS.
  • CAS may serve as a therapeutic target for tumor elimination, particularly in conjunction with agents that induce its expression.

More Related Videos

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF311:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

Using CRISPR/Cas9 Gene Editing to Investigate the Oncogenic Activity of Mutant Calreticulin in Cytokine Dependent Hematopoietic Cells10:21

Using CRISPR/Cas9 Gene Editing to Investigate the Oncogenic Activity of Mutant Calreticulin in Cytokine Dependent Hematopoietic Cells

Published on: January 5, 2018

Related Concept Videos

Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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...