Abstract
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), also known as Apo-2 ligand (Apo2L), is a member of the TNF cytokine superfamily. TRAIL has been widely studied as a novel strategy for tumor elimination, as cancer cells overexpress TRAIL death receptors, inducing apoptosis and inhibiting blood vessel formation. However, cancer stem cells (CSCs), which are the main culprits responsible for therapy resistance and cancer remission, can easily develop evasion mechanisms for TRAIL apoptosis. By further modifying their properties, they take advantage of this molecule to improve survival and angiogenesis. The molecular mechanisms that CSCs use for TRAIL resistance and angiogenesis development are not well elucidated. Recent research has shown that proteins and transcription factors from the cell cycle, survival, and invasion pathways are involved. This review summarizes the main mechanism of cell adaption by TRAIL to promote response angiogenic or pro-angiogenic intermediates that facilitate TRAIL resistance regulation and cancer progression by CSCs and novel strategies to induce apoptosis.
Highlights
IntroductionProgrammed cell death, is a naturally occurring mechanism that eliminates damaged cells
Apoptosis, or programmed cell death, is a naturally occurring mechanism that eliminates damaged cells
An example of an intrinsic pathway can be seen as induced by the B cell lymphoma 2 (Bcl-2)-regulated mitochondrial pathway, leading to a release of cytochrome c, which associates with apoptotic protease activating factor 1 (APAF-1) and pro-caspase-9, forming the apoptosome, leading to the activation of caspase-9 [3]
Summary
Programmed cell death, is a naturally occurring mechanism that eliminates damaged cells. The first receptors are overexpressed in tumors, and the latter are expressed mainly in normal cells [9] The difference between both receptor types is the lack of cytoplasmic domains required for apoptosis activation. Another receptor discovered to bind TRAIL is osteoprotegerin (OPG). Active caspases are proteolytic proteins that bench to cytosolic and nuclear targets; caspases cause cleavage of actin filaments of the cytoskeleton, the inhibitor of caspase-activated DNase (ICAD) that avoids activation of caspase-activated DNase (CAD) that destroys DNA [12] This mechanism of cell death, which has been widely studied in the context of cancer and other diseases, is efficient. Apoptosis continues to be a therapeutic target that needs to be studied
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