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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Triad 1 induces apoptosis by p53 activation
Jin Hyuk Jung1, Sun-Mi Lee, Seunghee Bae
1Functional Genome Research Institute, Konkuk University, Seoul, Republic of Korea.
FEBS Letters
|March 16, 2010
Summary
Triad 1, an E3 ligase, triggers cancer cell death (apoptosis) through its ligase activity. This process is p53-dependent, with Triad 1 enhancing p53 activity.
Area of Science:
- Molecular Biology
- Cancer Research
- Biochemistry
Background:
- Triad 1 (really interesting new gene) and double RING finger linked 1 is an E3 ligase.
- It is known to induce apoptosis and inhibit clonogenic growth in myeloid cells by stabilizing Gfi-1.
- The precise mechanisms by which Triad 1 induces apoptosis in various cancer cell lines remain to be fully elucidated.
Purpose of the Study:
- To investigate the role and mechanism of Triad 1 in inducing apoptosis in diverse cancer cell lines.
- To determine whether Triad 1-induced apoptosis in cancer cells is mediated by Gfi-1 stabilization or other pathways.
- To explore the relationship between Triad 1, p53, and apoptosis in cancer cells.
Main Methods:
- Utilizing various human cancer cell lines (MCF7, A549, U2OS, HCT 116 p53(+/+)).
- Assessing apoptosis induction by Triad 1 through its RING ligase activity.
- Investigating the involvement of p53 and Gfi-1 in Triad 1-mediated apoptosis.
- Analyzing Triad 1's effect on p53 transactivation.
Main Results:
- Triad 1 induces apoptosis in multiple cancer cell lines, including MCF7, A549, U2OS, and HCT 116 p53(+/+).
- Apoptosis induced by Triad 1 in these cancer cells is independent of Gfi-1 stabilization.
- Triad 1-induced apoptosis is dependent on p53 and promotes p53 transactivation.
Conclusions:
- Triad 1's ligase activity is sufficient to induce apoptosis in various cancer cell lines.
- The mechanism of Triad 1-induced apoptosis in cancer cells involves p53 activation, not Gfi-1 stabilization.
- Triad 1 represents a potential therapeutic target for inducing apoptosis in cancer via p53 activation.
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