Abstract
Cancer is a category of diseases involving abnormal cell growth with the potential to invade other parts of the body. Chemotherapy is the most widely used first-line treatment for multiple forms of cancer. Chemotherapeutic agents act via targeting the cellular apoptotic pathway. However, cancer cells usually acquire chemoresistance, leading to poor outcomes in cancer patients. For that reason, it is imperative to discover other cell death pathways for improved cancer intervention. Pyroptosis is a new form of programmed cell death that commonly occurs upon pathogen invasion. Pyroptosis is marked by cell swelling and plasma membrane rupture, which results in the release of cytosolic contents into the extracellular space. Currently, pyroptosis is proposed to be an alternative mode of cell death in cancer treatment. Accumulating evidence shows that the key components of pyroptotic cell death pathways, including inflammasomes, gasdermins and pro-inflammatory cytokines, are involved in the initiation and progression of cancer. Interfering with pyroptotic cell death pathways may represent a promising therapeutic option for cancer management. In this review, we describe the current knowledge regarding the biological significance of pyroptotic cell death pathways in cancer pathogenesis and also discuss their potential therapeutic utility.
Highlights
Cell death is a crucial phenomenon in biological activities and serves a pivotal role in maintaining homeostatic balance in vivo [1]
We summarize the recent findings related to the role and mechanism of pyroptotic cell death pathways in cancer progression and discuss potential therapeutic values in targeting pyroptosis for cancer therapy
Canonical pyroptosis is executed by caspase-1, which is triggered by a number of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), while non-canonical pyroptosis is dependent on human caspase-4/-5 or mouse caspase-11 and can be induced by intracellular LPS [20]
Summary
Cell death is a crucial phenomenon in biological activities and serves a pivotal role in maintaining homeostatic balance in vivo [1]. As a form of non-inflammatory programmed cell death, apoptosis can be induced by either intrinsic or extrinsic factors, followed by sequential activation of initiator and executioner caspases [3,4]. Both apoptosis and pyroptosis are executed by caspases. The non-canonical inflammasome pathway can be initiated by the direct binding of caspase-4, -5 and -11 to lipopolysaccharide (LPS) from Gram-negative bacteria [13] These caspases activate GSDMD to induce cell lysis and death. We summarize the recent findings related to the role and mechanism of pyroptotic cell death pathways in cancer progression and discuss potential therapeutic values in targeting pyroptosis for cancer therapy
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