Role of pyroptosis in cancer and its therapeutic regulation

Mamun, Abdullah Al; Mimi, Anjuman Ara; Aziz, Abdul; Zaeem, Muhammad; Ahmed, Tanvir; Munir, Fahad; Xiao, Jian

doi:10.1016/j.ejphar.2021.174444

Cited by 37 publications

(28 citation statements)

References 138 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Meanwhile, pyroptosis may mediate cell death by Caspase-1–dependent, Caspase-4/5/11–dependent, and Caspase-3/8–dependent inflammasome signaling pathways ( Antonopoulos et al, 2015 ; Yu et al, 2019 ; Chen et al, 2020 ; Liu et al, 2021 ; L.; Wang et al, 2021 ). Recently, increasing studies show that pyroptosis is associated with the development of cancer ( Al Mamun et al, 2021 ). Wang et al indicted that 5-FU can induce pyroptosis in gastric cancer cell by Caspase-3 signaling pathways ( Wang et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

“…After cell rupture, proinflammatory cytokines and immunogenic substances are released to promote immune cell activation and infiltration, which may result in a strong inflammatory response and significant tumor regression ( Wang et al, 2017 ; Loveless et al, 2021 ). Increasing studies indicated that pyroptosis may play important roles in the development of many cancers ( Al Mamun et al, 2021 ). In COAD, pyroptosis may participate in the tumorigenesis of cancer ( Tan et al, 2020 ; Tang et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of the Pyroptosis-Related Gene Signature and Risk Score Model for Colon Adenocarcinoma

et al. 2021

View full text Add to dashboard Cite

The prognosis of advanced colon adenocarcinoma (COAD) remains poor. However, existing methods are still difficult to assess patient prognosis. Pyroptosis, a lytic and inflammatory process of programmed cell death caused by the gasdermin protein, is involved in the development and progression of various tumors. Moreover, there are no related studies using pyroptosis-related genes to construct a model to predict the prognosis of COAD patients. Thus, in this study, bioinformatics methods were used to analyze the data of COAD patients downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to construct a risk model for the patient prognosis. TCGA database was used as the training set, and GSE39582 downloaded from GEO was used as the validation set. A total of 24 pyroptosis-related genes shown significantly different expression between normal and tumor tissues in COAD and seven genes (CASP4, CASP5, CASP9, IL6, NOD1, PJVK, and PRKACA) screened by univariate and LASSO cox regression analysis were used to construct the risk model. The receiver operating characteristic (ROC) and Kaplan–Meier (K–M curves) curves showed that the model based on pyroptosis-related genes can be used to predict the prognosis of COAD and can be validated by the external cohort well. Then, the clinicopathological factors were combined with the risk score to establish a nomogram with a C-index of 0.774. In addition, tissue validation results also showed that CASP4, CASP5, PRKACA, and NOD1 were differentially expressed between tumor and normal tissues from COAD patients. In conclusion, the risk model based on the pyroptosis-related gene can be used to assess the prognosis of COAD patients well, and the related genes may become the potential targets for treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identification of the Pyroptosis-Related Gene Signature and Risk Score Model for Colon Adenocarcinoma

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Pyroptosis was initially an important pathway to antagonize cell infection, and with the deepening of research, it was found to play a linchpin role in influencing the tumor microenvironment (TME) (Ye et al, 2021). Accumulating evidence has indicated that pyroptosis impacts the prognosis of patients in multiple cancers by promoting or inhibiting the proliferation, invasion, and metastasis of tumors (Fang et al, 2020;Al Mamun et al, 2021;Lin et al, 2021). For instance, recent research revealed that pyroptosis promoted the proliferation of esophageal squamous carcinoma cells through the PKM2-caspase-8/3-GSDME pathway (Jiang et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

“…Long non-coding RNAs (lncRNAs), a type of non-coding RNA molecules greater than 200 nucleotides in length, play important roles in regulating the transcriptional, posttranscriptional, or epigenetic level (Al Mamun et al, 2021). Emerging evidence has indicated that the interactions between pyroptosis and lncRNAs are significant in the development of multiple complex human diseases, especially in cancers (He et al, 2020;Gao et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Integrated Analysis of Multi-Omics Alteration, Immune Profile, and Pharmacological Landscape of Pyroptosis-Derived lncRNA Pairs in Gastric Cancer

Guo

Yin

Liu

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Background: Recent evidence demonstrates that pyroptosis-derived long non-coding RNAs (lncRNAs) have profound impacts on the initiation, progression, and microenvironment of tumors. However, the roles of pyroptosis-derived lncRNAs (PDLs) in gastric cancer (GC) remain elusive.Methods: We comprehensively analyzed the multi-omics data of 839 GC patients from three independent cohorts. The previous gene set enrichment analysis embedding algorithm was utilized to identify PDLs. A gene pair pipeline was developed to facilitate clinical translation via qualitative relative expression orders. The LASSO algorithm was used to construct and validate a pyroptosis-derived lncRNA pair prognostics signature (PLPPS). The associations between PLPPS and multi-omics alteration, immune profile, and pharmacological landscape were further investigated.Results: A total of 350 PDLs and 61,075 PDL pairs in the training set were generated. Cox regression revealed 15 PDL pairs associated with overall survival, which were utilized to construct the PLPPS model via the LASSO algorithm. The high-risk group demonstrated adverse prognosis relative to the low-risk group. Remarkably, genomic analysis suggested that the lower tumor mutation burden and gene mutation frequency (e.g., TTN, MUC16, and LRP1B) were found in the high-risk group patients. The copy number variants were not significantly different between the two groups. Additionally, the high-risk group possessed lower immune cell infiltration abundance and might be resistant to a few chemotherapeutic drugs (including cisplatin, paclitaxel, and gemcitabine).Conclusion: PDLs were closely implicated in the biological process and prognosis of GC, and our PLPPS model could serve as a promising tool to advance prognostic management and personalized treatment of GC patients.

show abstract

“…Pyroptosis directly assembles the inflammasome (NLRP3) by damage-associated molecular pattern (DAMP) and activates the cysteine protease caspase-1, allowing the translocation of the N-terminal domain fragment of the GasderminD (GSDMD) protein to the cell membrane to form β-barrel transmembrane pores ( 17 ). Hence, the plasma membranes were rapidly ruptured to release cellular contents and a large number of inflammatory factors, and send proinflammatory signals to adjacent cells to recruit inflammatory cells and induce an inflammatory response, eventually causing cell death ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of HMGB1 Ameliorates the Maternal-Fetal Interface Destruction in Unexplained Recurrent Spontaneous Abortion by Suppressing Pyroptosis Activation

et al. 2021

View full text Add to dashboard Cite

Recurrent spontaneous abortion (RSA) is a common complication of pregnancy that affects the physical and mental health of pregnant women, and approximately 50% of the mechanisms are unclear. Our previous studies have found that high mobility group box 1 (HMGB1) molecules are highly expressed at the maternal-fetal interface of unexplained recurrent spontaneous abortion (URSA) patients. The purpose of this study was to further detect the expression of HMGB1 and pyroptosis in decidual tissue of URSA patients, and explore the potential mechanism of the protective role of HMGB1 in URSA patients and mouse model. The decidua tissues of 75 URSA patients and 75 women who actively terminated pregnancy were collected, and URSA mouse models were established and treated with HMGB1 inhibitor-aspirin. The expression of HMGB1, and their receptors (RAGE, TLR2, TLR4), pyroptosis-associated proteins (NLRP-3, caspase-1, GSDMD) and NF-κB was examined at the maternal-fetal interface of human and mouse. Our study found that HMGB1, NLRP-3, Caspase-1, GSDMD, RAGE, TLR2 and TLR4 were highly expressed and NF-κB signaling pathway were activated in the decidua tissue of URSA group. Moreover, immune cell disorder and co-localization of HMGB1 and macrophages were found at the maternal-fetal interface of URSA mice. However, HMGB1, TLR2, TLR4, NF-κB, and pyroptosis-associated proteins can be down-regulated by administering low-dose aspirin. These data may indicate that highly expressed HMGB1 was actively secreted by macrophages and then activated pyroptosis through the TLR2/TLR4-NF-κB pathway to cause aseptic inflammation, leading to the occurrence and development of URSA. Moreover, low-dose aspirin can reduce HMGB1 protein levels of serum and decidual in URSA.

show abstract

Role of pyroptosis in cancer and its therapeutic regulation

Cited by 37 publications

References 138 publications

Identification of the Pyroptosis-Related Gene Signature and Risk Score Model for Colon Adenocarcinoma

Identification of the Pyroptosis-Related Gene Signature and Risk Score Model for Colon Adenocarcinoma

Integrated Analysis of Multi-Omics Alteration, Immune Profile, and Pharmacological Landscape of Pyroptosis-Derived lncRNA Pairs in Gastric Cancer

Inhibition of HMGB1 Ameliorates the Maternal-Fetal Interface Destruction in Unexplained Recurrent Spontaneous Abortion by Suppressing Pyroptosis Activation

Contact Info

Product

Resources

About