Apoptosis induction in cancer cells Overview
Apoptosis induction in cancer cells" refers to the process of triggering programmed cell death specifically within malignant cells. This is not a single molecule or receptor, but rather a complex cellular outcome involving multiple molecular targets and pathways. Key effectors include mitochondrial proteins such as cytochrome c, members of the Bcl-2 family, caspases (especially caspase-9 and caspase-3), and regulatory factors like Apaf‑1. Many anticancer drugs exert their effects by activating these apoptotic pathways—either through direct DNA damage that signals via p53 or by targeting anti-apoptotic proteins downstream when p53 is mutated or inactive. Direct pharmacological activation of core apoptosis machinery has been explored as a strategy to selectively kill cancer cells while sparing normal tissue; however, "apoptosis induction" itself does not represent a discrete druggable target but rather an overarching therapeutic goal achieved by modulating specific molecules within this pathway. Because "apoptosis induction in cancer cells" describes a process rather than an individual protein or receptor, it cannot be assigned standard target attributes such as canonical name or abbreviation. It should not be considered a valid therapeutic target entry on its own.
Mechanism of Action
Activation of caspases via cytochrome c-dependent pathways; Promotion of apoptosome formation (Apaf-1 oligomerization)
Biological Functions
Disease Associations
Safety Considerations
- Potential for resistance due to mutations in apoptosis pathway components (e.g., p53 mutation)
Interacting Drugs
Associated Biomarkers
Biomarker |
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Caspase activation status |
Cytochrome c release |