Expression levels of caspase‐3 and gasdermin E and their involvement in the occurrence and prognosis of lung cancer

Huang, Yuan‐Li; Zhang, Guanghui; Zhu, Qing; Wu, Xia; Wu, Ligao

doi:10.1002/cnr2.1561

Cited by 18 publications

(7 citation statements)

References 33 publications

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“…In lung cancer, the balance between cell death and cell division is disrupted, leading to the uncontrolled growth and proliferation of cancer cells. Research has shown that the levels of caspase-9 are often decreased in lung cancer cells, which may contribute to the resistance of these cells to apoptosis (Huang et al 2022;Li et al 2022). BaP induced lung cancer mice exhibited suppressed level of caspase-3 and caspase-9 and metformin and atorvastatin combination treatment remarkably restored the level.…”

Section: Discussionmentioning

confidence: 99%

Combination therapy of metformin and atorvastatin against benzopyrene-induced lung cancer via inflammatory signaling pathway

Ning,

Zhang,

Gao

et al. 2024

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The most prevalent cause of lung cancer is smoking tobacco, but exposure to second hand smoke, air pollution, and certain chemicals and substances at work can also raise the risk of disease. In this study, we scrutinized the chemoprotective effect of the metformin and atorvastatin combination against benzo[a]pyrene (BaP)-induced lung cancer in mice of Swiss albino. BaP (50 mg/kg) was used for induction of lung cancer and mice were treated with metformin, atorvastatin or their combination. Metformin + atorvastatin combination significantly (p < 0.001) improved the body weight, liver weight, suppressed the lung weight and tumor incidence and altered the levels of immunocompetent cells, polyamines, lung tumor markers, lung parameters and antioxidant parameters, respectively. Metformin + atorvastatin combination also suppressed cytokines levels, inflammatory parameters and caspase parameters. On the basis of the results, we can conclude that metformin + atorvastatin combination remarkably suppressed lung cancer via the inflammatory pathway.

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Section: Discussionmentioning

confidence: 99%

Combination therapy of metformin and atorvastatin against benzopyrene-induced lung cancer via inflammatory signaling pathway

Ning,

Zhang,

Gao

et al. 2024

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“…Previous research has shown that both N-GSDME and N-GSDMD can augment caspase 3/7-mediated apoptotic cell death in cancer cells by promoting release of proapoptotic proteins like cytochrome C from mitochondria 108 . GSDMD has also been shown to target mitochondria following intracellular LPS-dependent activation of caspase 11 in endothelial cells 129 . In this context, N-GSDMD promotes mtDNA release and cGAS/STING activation in the absence of cell death, suggesting that redistribution of GSDMD to and from the mitochondria may constitute an important node in regulating cell death outcomes.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction promotes alternative gasdermin D-mediated inflammatory cell death and susceptibility to infection

Weindel

Zhao

Martinez

et al. 2021

Preprint

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SUMMARYHuman mutations in mitochondrial-associated genes are associated with inflammatory diseases and susceptibility to infection. However, their mechanistic contributions to immune outcomes remain ill-defined. We discovered that the disease-associated gain-of-function allele Lrrk2G2019S (leucine-rich repeat kinase 2) promotes mitochondrial hyper-fission, depolarization, and oxidative stress in macrophages. In the presence of Lrrk2G2019S-dependent mitochondrial perturbations, AIM2 inflammasome activation promotes more cell death but not more pyroptotic IL-1b release. Instead, inflammasome activation in Lrrk2G2019S macrophages triggers gasdermin D (GSDMD)-mediated mitochondrial pores, driving up ROS-mediated RIPK1/RIPK3/MLKL dependent necroptosis. Consequently, infection of Lrrk2G2019S mice with Mycobacterium tuberculosis elicits hyperinflammation and immunopathology via enhanced neutrophil infiltration. By uncovering that GSDMD promotes non-pyroptotic cell death in Lrrk2G2019S macrophages, our findings demonstrate that altered mitochondrial function can reprogram cell death modalities to elicit distinct immune outcomes. This provides mechanistic insights into why mutations in LRRK2 are associated with susceptibility to chronic inflammatory and infectious diseases.HIGHLIGHTSAltered mitochondrial homeostasis reprograms cell death modalitiesGSDMD associates with and depolarizes mitochondrial membranes following AIM2 activationGSDMD initiates a shift from pyroptotic to necroptotic cell death in Lrrk2G2019S macrophagesLrrk2G2019S elicits hyperinflammation and susceptibility to infection in flies and mice

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“…GSDME, caspase 3, and caspase 8 are more abundantly expressed in tumor tissue. Elevated GSDME expression is associated with a higher postoperative survival rate and a lower lymph node metastasis rate, which suggests that it may serve as a predictor of prognosis in lung cancer patients 124 . LUAD prognosis is also associated with new pyroptosis‐related prognostic markers, including NOD1, NLRP1, NLRP2, NLRP7, and caspase 6.…”

Section: Pyroptosis and Inflammasomes In Cancermentioning

confidence: 99%

“…Elevated GSDME expression is associated with a higher postoperative survival rate and a lower lymph node metastasis rate, which suggests that it may serve as a predictor of prognosis in lung cancer patients. 124 LUAD prognosis is also associated with new pyroptosis‐related prognostic markers, including NOD1, NLRP1, NLRP2, NLRP7, and caspase 6. The notion that pyroptosis can mediate the TME to exert an antitumor effect is supported by these genes, which are intimately linked to immune infiltration.…”

Section: Pyroptosis and Inflammasomes In Cancermentioning

confidence: 99%

Pyroptosis and inflammasomes in cancer and inflammation

Wang,

Hua,

Bao

et al. 2023

MedComm

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Nonprogrammed cell death (NPCD) and programmed cell death (PCD) are two types of cell death. Cell death is significantly linked to tumor development, medication resistance, cancer recurrence, and metastatic dissemination. Therefore, a comprehensive understanding of cell death is essential for the treatment of cancer. Pyroptosis is a kind of PCD distinct from autophagy and apoptosis in terms of the structure and function of cells. The defining features of pyroptosis include the release of an inflammatory cascade reaction and the expulsion of lysosomes, inflammatory mediators, and other cellular substances from within the cell. Additionally, it displays variations in osmotic pressure both within and outside the cell. Pyroptosis, as evidenced by a growing body of research, is critical for controlling the development of inflammatory diseases and cancer. In this paper, we reviewed the current level of knowledge on the mechanism of pyroptosis and inflammasomes and their connection to cancer and inflammatory diseases. This article presents a theoretical framework for investigating the potential of therapeutic targets in cancer and inflammatory diseases, overcoming medication resistance, establishing nanomedicines associated with pyroptosis, and developing risk prediction models in refractory cancer. Given the link between pyroptosis and the emergence of cancer and inflammatory diseases, pyroptosis‐targeted treatments may be a cutting‐edge treatment strategy.

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Expression levels of caspase‐3 and gasdermin E and their involvement in the occurrence and prognosis of lung cancer

Cited by 18 publications

References 33 publications

Combination therapy of metformin and atorvastatin against benzopyrene-induced lung cancer via inflammatory signaling pathway

Combination therapy of metformin and atorvastatin against benzopyrene-induced lung cancer via inflammatory signaling pathway

Mitochondrial dysfunction promotes alternative gasdermin D-mediated inflammatory cell death and susceptibility to infection

Pyroptosis and inflammasomes in cancer and inflammation

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