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Updated: Aug 5, 2026
10:03
Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy
Published on: August 2, 2024
ASK1 in Cancer Cell Death: Insights from In Vitro and In Vivo Studies
Eric J O'Neill1, Amanda Kornel1, Emily C Irwin1
1Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada.
Cells
|July 27, 2026
Summary
Apoptosis signal-regulating kinase 1 (ASK1) is crucial for stress-induced cancer cell death. Activating ASK1 shows promise for developing new anticancer therapies targeting various cancers.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Apoptosis signal-regulating kinase 1 (ASK1) is a MAP3K involved in stress-induced apoptosis.
- ASK1 activation is linked to the anticancer effects of various compounds, especially those inducing oxidative or ER stress.
Purpose of the Study:
- To review studies demonstrating ASK1-dependent apoptosis in various cancer models.
- To focus on mechanistic evidence linking ASK1 to downstream pathways and cell death.
Main Methods:
- Literature review of studies with experimental validation of ASK1 activation.
- Analysis of mechanistic evidence connecting ASK1 to JNK/p38 MAPK pathways, mitochondrial dysfunction, and caspase-dependent cell death.
Main Results:
- ASK1 activation mediates anticancer effects of natural products, phytochemicals, and synthetic agents.
- ASK1 triggers downstream JNK and p38 MAPK activation, leading to mitochondrial dysfunction and apoptosis.
Conclusions:
- ASK1 is a key mediator of anticancer effects induced by various agents.
- ASK1 represents a promising molecular target for novel cancer treatment strategies.
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