Induction of apoptosis in tumor cells

"Induction of apoptosis in tumor cells" is not a specific molecular target but rather a **therapeutic strategy** aimed at selectively triggering programmed cell death pathways within cancerous cells. Apoptosis can be initiated through two main signaling cascades: 1. **Extrinsic pathway**—mediated by cell surface death receptors such as TNFR1, DR4, and DR5 that bind ligands like TRAIL or TNFα. This leads to the formation of the death-inducing signaling complex (DISC), recruitment and activation of initiator caspases like caspase‑8, which then activate effector caspases resulting in cellular dismantling. 2. **Intrinsic pathway**—regulated by mitochondrial signals involving the Bcl‑2 protein family. Pro-apoptotic members like Bax and Bak promote mitochondrial outer membrane permeabilization, releasing cytochrome c into the cytosol and activating downstream effector caspases via apoptosome formation. Both pathways converge on executioner caspases that orchestrate cellular breakdown. Many anticancer drugs aim to restore or enhance these apoptotic processes by targeting key regulatory proteins such as p53, Bcl‑2 family members, inhibitor-of-apoptosis proteins (IAPs), or directly activating death receptors. Because "induction of apoptosis" describes a process rather than a discrete molecule/receptor/protein entity with defined structure/function relationships typical for drug targets, it is not considered a canonical therapeutic target itself but encompasses multiple validated molecular targets within its scope[2][4][5].

Activation of death receptors (extrinsic pathway) leading to caspase activation - Disruption of mitochondrial membrane integrity (intrinsic pathway) via Bcl-2 family modulation - Inhibition of anti-apoptotic proteins such as Bcl‑2 or IAPs[2][4][5][9]