Apoptosis induction in neoplastic cells

"Apoptosis induction in neoplastic cells" refers broadly to the therapeutic strategy and biological phenomenon whereby programmed cell death is triggered specifically within cancerous tissues. Apoptosis can be initiated via two main routes—the intrinsic mitochondrial pathway involving pro-apoptotic factors like Bax and cytochrome c release leading to activation of initiator and effector caspases; and the extrinsic pathway mediated by engagement of surface 'death receptors' such as Fas/TNF/TRAIL receptors which also converge on downstream caspase activation. Many anti-cancer agents—including chemotherapeutics like gemcitabine and natural products such as fucoidan—exert their effects at least partly through promoting apoptotic signaling cascades within tumor cells. However, 'apoptosis induction' itself is not a discrete druggable entity but rather an outcome resulting from modulation of diverse molecular targets.

Other names

Induction of apoptosis in tumor cellsTumor cell apoptosis inductionCancer cell apoptosis

Drugs that induce apoptosis typically act by: - Activating intrinsic mitochondrial pathways (e.g., upregulating pro-apoptotic Bcl‑2 family proteins like Bax) - Engaging extrinsic death receptor pathways (e.g., Fas ligand binding) - Direct activation of caspases such as caspase 3/7/8/9