Molecular Classification
Other
Disease Roles
Cancer

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

Apoptosis
Cell death
Cancer cell elimination

Disease Associations

Cancer

Safety Considerations

  • Potential for resistance due to mutations in apoptosis pathway components (e.g., p53 mutation)

Interacting Drugs

Many chemotherapeutic drugs (e.g., DNA-damaging agents, Bcl-2 inhibitors)

Associated Biomarkers

Biomarker
Caspase activation status
Cytochrome c release