The Modulation of Cancer Progression and Antitumor Immunity by Pyroptosis

Journal of Oncology Medicine & Practice

ISSN: 2576-3857

Open Access

Opinion - (2022) Volume 7, Issue 3

The Modulation of Cancer Progression and Antitumor Immunity by Pyroptosis

Stephen Wang*
*Correspondence: Stephen Wang, Department of Radiation Oncology, University Hospital Bonn, Bonn, Germany, Email:
Department of Radiation Oncology, University Hospital Bonn, Bonn, Germany

Received: 08-Jun-2022, Manuscript No. jomp-22-74704; Editor assigned: 13-Jun-2022, Pre QC No. P-74704; Reviewed: 23-Jun-2022, QC No. Q-74704; Revised: 26-Jun-2022, Manuscript No. R-74704; Published: 30-Jun-2022 , DOI: 10.37421/2157-7145.2022.7.163
Citation: Wang, Stephen. “The Modulation of Cancer Progression and Antitumor Immunity by Pyroptosis” J Oncol Med & Pract 7 (2022): 163.
Copyright: © 2022 Wang S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


To sustain in vivo stability throughout organismal growth and development, cell death is essential. There are two categories of cell death: accidental cell death and purposeful cell death. By-accident cell death is brought on by noxious physical, chemical, or mechanical stimuli that are not properly controlled. PCD, on the other hand, is a form of protective suicide that kills out undesirable or aberrant cells while promoting morphogenesis. Pyroptosis is a pro-inflammatory PCD used to combat infection and endogenous danger signals. It is sometimes referred to as cell inflammatory necrosis. The two types of pyroptosis are canonical pyroptosis, which depends on caspase-1, and non-canonical pyroptosis, which does not. Inflammation is linked to numerous cancers, including non-small cell lung cancer colorectal cancer, gastric cancer, and hepatocellular carcinoma. Additional research on pyroptosis is advantageous for treating neurological illnesses as well. Although the connection between pyroptosis and antitumor immunity is still unknown, studies have demonstrated that pyroptosis promotes immune cell activity, which in turn promotes tumour regression. While immune cell pyroptosis is in responsibility of a host's protection against a pathogen infection, cancer cell biological mutation increases inflammatory reactions in the tumour microenvironment, which successfully encourages antitumor immunity. Together, CCP and ICP have an impact on the growth of tumours. Pyroptosis, a two-edged sword during carcinogenesis, is currently under debate. A thorough comprehension of pyroptosis in the tumour cells will aid in the creation of fresh and successful cancer treatment options [1].

Chromatin condensation, cell membrane rupture, endoplasmic reticulum expansion, and the production of IL-1 as an inflammatory response were all mentioned in descriptions of the phenomena known as pyroptosis. The first identification and naming of the effector of pyroptosis occurred in 2000. Before Brennan and Cookson discovered that macrophages infected with Salmonella typhimurium perished through an inflammatory death mechanism as opposed to the conventional type of apoptosis, pyroptosis was thought to be a particular type of apoptotic cell death in monocytes. Pyroptosis is characterised by its rapid onset, rapid destruction of the cell membrane's integrity, and strong inflammatory reaction. However, this important finding went unnoticed at the time, and the precise chemical mechanism of pyroptosis is still unknown [2]. An attempt was made to replace the word "caspase-activating complex," which initiates the inflammatory caspases. Pyroptosis, an inflammatory cell death, is crucial for the development of both immunity and malignancy. Pyroptosis may affect carcinogenesis differently depending on the surroundings and resulting in radically different outcomes when treating cancer. The traditional cancer treatment options include chemotherapy and radiation. However, both cancer cells and healthy cells, including immune cells, are promptly eliminated by these treatments. Immunotherapy activates the body's natural defences to destroy cancer cells. Cancer cells can use ESCRT-mediated membrane repair to avoid the immune system's "search" for them. The CHMP4B deletion improved the ability of CTLs to destroy cancer cells by inhibiting the ESCRT pathway [3].

Additionally, our study team identified five PRGs that may further improve immunotherapy and developed a novel technique to predict cancer patient survival and immunotherapy outcomes from the standpoint of pyroptosis. Pyroptosis modifies the tumour microenvironment and slows tumour growth by producing inflammatory molecules like IL-1 and IL-18, but it also lessens the body's immunological responses to tumour cells and speeds up the growth of many cancers. Apoptosis eliminates damaged and faulty cells to maintain the organism's health under physiological circumstances [4]. The process of tissue remodelling, biological growth, and development all involve apoptosis. Apoptosis is a Greek word that translates to "flower petals falling off, tree leaves falling off." There are unique aspects in the cell morphology after apoptosis has taken place. First, nuclear fragmentation and chromatin condensation take place. Apoptotic bodies, which contain an intact cytoplasm with a complete membrane, organelles, and nuclear fragments, emerge from the surface of the cell membrane next.

Ferroptosis is brought on by lipid peroxidation that is iron-dependent. Ferroptosis differs from apoptosis and pyroptosis in that it takes place without chromatin condensation and without the need for caspase. Ferroptosis has a representative morphological trait called mitochondrial atrophy. The nucleus is unharmed, and ferroptosis and inflammatory reactions take place, which is consistent with pyroptosis. By removing lipid peroxides, Glutathione Peroxidase 4 (GPX4), a crucial player in the control of ferroptosis, preserves metabolic equilibrium. If the expression of GPX4 is suppressed, ferroptosis will result [5]. Reactive oxygen species, iron concentration, and metabolic rate are all higher in cancer cells than in healthy cells. According to the aforementioned characteristics, ferroptosis in cancer cells can slow the growth of tumours.


In contrast to apoptosis and ferroptosis, pyroptosis is accompanied by a cell rupture and a significant inflammatory response. Here, we gave a thorough overview of pyroptosis and talked about how it relates to the development of cancer. First, a variety of stimulation signals, such as PAMPs, DAMPs, pharmacological stimulations, and granzymes, can initiate pyroptosis. The majority of stimuli are communicated by activating granzymes and caspases, which then activate gasdermins. The gasdermin N-terminus, which punches the cell membrane, is then exposed when active caspases or granzymes have cleaved the gasdermin. IL-1 and IL-18, which are intracellular inflammatory mediators, are released during pyroptosis to cause inflammation and cell death. Studies have increasingly indicated that pyroptosis and cancer are closely related. However, it is currently unclear how pyroptosis and cancer are related.

On the one hand, pyroptosis can successfully control the tumour immunological milieu, trigger a potent T cell-mediated antitumor immune response, suppress tumour development, and improve the sensitivity of cancer cells to chemotherapeutic medicines. On the other hand, because pyroptosis is a cell death process that promotes inflammation, it also offers a favourable milieu for the development of tumours. Studying the mechanism of pyroptosis can therefore lead to the development of fresh cancer therapy plans. Because pyroptosis is a key component of tumour immunity and tumour immunotherapy, the relationship between pyroptosis and tumour immunity also offers significant insights into cancer drugs.


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