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      Application of pyroptosis in tumor research (Review)

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          Abstract

          As a potent clinical strategy, cancer therapy has sparked an academic boom over the past few years. Immune checkpoint inhibitors (ICIs) have been demonstrated to be highly successful. These achievements have progressed cancer treatment and have made an indelible mark on cancer. However, the inherent complexity of cancer means that only part of the population can benefit from this treatment. Pyroptosis is a new suicidal cellular mechanism that induces inflammation by releasing immunogenic cellular components. Inflammatory signaling cascades mediated by pyroptosis commonly inspire numerous cell lysis in immune diseases. Contrariwise, this consequence may be a promising target in cancer research. Therefore, the present study briefly described programmed cell death processes and their potential roles in cancer. Because of the rapid development of bioengineering in cancer, the present study also examined the associated scaffolding available for cancer, highlighting advances in tumor engineering approaches. Ultimately, an improved understanding of pyroptosis and tumor scaffolding might shed light on a combination that can be manipulated for therapeutic purposes.

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          Most cited references114

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Oncology meets immunology: the cancer-immunity cycle.

            The genetic and cellular alterations that define cancer provide the immune system with the means to generate T cell responses that recognize and eradicate cancer cells. However, elimination of cancer by T cells is only one step in the Cancer-Immunity Cycle, which manages the delicate balance between the recognition of nonself and the prevention of autoimmunity. Identification of cancer cell T cell inhibitory signals, including PD-L1, has prompted the development of a new class of cancer immunotherapy that specifically hinders immune effector inhibition, reinvigorating and potentially expanding preexisting anticancer immune responses. The presence of suppressive factors in the tumor microenvironment may explain the limited activity observed with previous immune-based therapies and why these therapies may be more effective in combination with agents that target other steps of the cycle. Emerging clinical data suggest that cancer immunotherapy is likely to become a key part of the clinical management of cancer. Copyright © 2013 Elsevier Inc. All rights reserved.
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              The NLRP3 inflammasome: molecular activation and regulation to therapeutics

              NLRP3 (NACHT, LRR and PYD domains-containing protein 3) is an intracellular sensor that detects a broad range of microbial motifs, endogenous danger signals and environmental irritants, resulting in the formation and activation of the NLRP3 inflammasome. Assembly of the NLRP3 inflammasome leads to caspase-1-dependent release of the proinflammatory cytokines, IL-1β and IL-18, as well as to gasdermin D-mediated pyroptotic cell death. Recent studies have revealed new regulators of the NLRP3 inflammasome, including new interacting or regulatory proteins, metabolic pathways and a regulatory mitochondrial hub. In this Review, we present the molecular, cell biological and biochemical basis of NLRP3 activation and regulation, and describe how this mechanistic understanding is leading to potential therapeutics that target the NLRP3 inflammasome.
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                Author and article information

                Journal
                Oncol Lett
                Oncol Lett
                OL
                Oncology Letters
                D.A. Spandidos
                1792-1074
                1792-1082
                September 2023
                18 July 2023
                18 July 2023
                : 26
                : 3
                : 376
                Affiliations
                [1 ]Department of Neurology, Changshu No. 2 People's Hospital, Affiliated Changshu Hospital of Nantong University, Suzhou, Jiangsu 215500, P.R. China
                [2 ]Basic Research Laboratory, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China
                Author notes
                Correspondence to: Ms. Jianing Tan, Department of Neurology, Changshu No. 2 People's Hospital, Affiliated Changshu Hospital of Nantong University, 18 Taishan Road, Changshu, Suzhou, Jiangsu 215500, P.R. China, E-mail: janietjn@ 123456163.com
                Article
                OL-26-3-13962
                10.3892/ol.2023.13962
                10407856
                37559585
                3185333e-5b13-4f6e-87b3-f1e03dbcc2b7
                Copyright: © Tan et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 12 May 2023
                : 27 June 2023
                Funding
                Funding: No funding was received.
                Categories
                Review

                Oncology & Radiotherapy
                pyroptosis,immune checkpoint inhibitors,tumor,inflammatory signaling cascades

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