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The term "antiapoptotic pathways" refers not to a specific molecule or receptor but rather a collection of cellular signaling mechanisms that prevent programmed cell death (apoptosis) and promote cell survival. These include the actions and regulation by various protein families—most notably the BCL‑2 family, inhibitor-of-apoptosis proteins (IAPs), PI3K/Akt/mTOR cascade, and transcriptional regulators like NF-kB. These networks function by inhibiting pro-death signals at multiple points within both intrinsic and extrinsic apoptotic cascades. Overactivation is commonly observed in cancer cells where it contributes significantly to tumor progression and therapeutic resistance. Because "antiapoptotic pathways" is not itself a discrete molecular entity but an umbrella term for many targets/processes involved in blocking apoptosis, it is not considered an individual therapeutic target; rather, its constituent molecules are targeted individually by various drugs.
Drugs targeting anti-apoptotic pathways typically: - Inhibit anti-apoptotic proteins such as Bcl-2/Bcl-xL/Mcl‑1, restoring the ability for pro-apoptotic signals to induce apoptosis. - Block signaling cascades like PI3K/Akt or NF-kB that promote expression/activation of anti-apoptotic factors. - Mimic pro-death BH3-only proteins to neutralize anti-apoptotic Bcl‑2 family members.
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