Exploration of induced sputum BIRC3 levels and clinical implications in asthma

Du, Lijuan; Xu, Changyi; Zeng, Zhimin; Chen, Fengjia; Tang, Kun; Liang, Yucheng; Guo, Yubiao

doi:10.1186/s12890-022-01887-2

Cited by 8 publications

(6 citation statements)

References 34 publications

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“…BIRC3 plays a role in protecting cells from apoptosis when exposed to proinflammatory cytokines. It has been demonstrated that BIRC3 protein expression increased noticeably in primary nasal epithelial cells when exposed to IFN-γ or TNF-α [25]. Our discovery also revealed that BIRC3 was up-regulated by cytokines such as TNFα and IL-1β (Figures 3 and 4), which confirmed that BIRC3 was the key mediator in inflammatory and immunity processes.…”

Section: Discussionsupporting

confidence: 78%

Expression Analysis of BIRC3 as One Target Gene of Transcription Factor NF-κB for Esophageal Cancer

Luo

Zhu

et al. 2022

Processes

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Esophageal cancer (ESCA) is one of the highest lethal malignancy tumors worldwide. Baculoviral IAP repeat-containing protein 3 (BIRC3) is the main inhibitor of apoptosis in many malignancies. The aim of this study was to clarify how BIRC3 acts in ESCA cells. Through TNMplot and GEPIA2 analysis, BIRC3 was found abundantly expressed in ESCA cells. The quantitative RT-PCR assay confirmed BIRC3 was pronouncedly induced in all used ESCA cell lines. In addition, proinflammatory cytokines TNFα and IL-1β were shown to have promotion effects on BIRC3 expression in ESCA cells. These promotive effects were blocked when the function of NF-κB was inhibited by bay 11-7082, which indicates the expression of the BIRC3 gene was regulated via the NF-κB transcription pathway in ESCA. Moreover, bioinformatics analysis showed that the BIRC3 gene had many NF-κB binding cis-elements. Chromatin immunoprecipitation was then performed and it was found that NF-κB directly interacts with cis-elements of the BIRC3 gene. In conclusion, our data proved that the high expression level of BIRC3 maintained the survival of ESCA cells. BIRC3 was up-regulated by proinflammatory cytokine TNFα and IL-1β through the NF-κB signaling pathway, and this may be helpful for esophageal cancer prevention and therapy.

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Section: Discussionsupporting

confidence: 78%

Expression Analysis of BIRC3 as One Target Gene of Transcription Factor NF-κB for Esophageal Cancer

Luo

Zhu

et al. 2022

Processes

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“…Studies have indicated that BIRC3 regulates immune-related lung diseases, including asthma and Klebsiella pneumoniae pneumonia. Increased BIRC3 expression may contribute to asthma pathogenesis by influencing eosinophilic and allergic inflammation ( 53 ). In a mouse model of infection, blocking the Birc3/TLR4/Myd88 signaling pathway showed a protective effect against carbapenem-resistant K. pneumoniae ( 54 ).…”

Section: Discussionmentioning

confidence: 99%

Comprehensive analysis of an endoplasmic reticulum stress-related gene prediction model and immune infiltration in idiopathic pulmonary fibrosis

Zhu,

Zhou,

Zhang

et al. 2024

Front. Immunol.

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BackgroundIdiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease. This study aimed to investigate the involvement of endoplasmic reticulum stress (ERS) in IPF and explore its correlation with immune infiltration.MethodsERS-related differentially expressed genes (ERSRDEGs) were identified by intersecting differentially expressed genes (DEGs) from three Gene Expression Omnibus datasets with ERS-related gene sets. Gene Set Variation Analysis and Gene Ontology were used to explore the potential biological mechanisms underlying ERS. A nomogram was developed using the risk signature derived from the ERSRDEGs to perform risk assessment. The diagnostic value of the risk signature was evaluated using receiver operating characteristics, calibration, and decision curve analyses. The ERS score of patients with IPF was measured using a single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm. Subsequently, a prognostic model based on the ERS scores was established. The proportion of immune cell infiltration was assessed using the ssGSEA and CIBERSORT algorithms. Finally, the expression of ERSRDEGs was validated in vivo and in vitro via RT-qPCR.ResultsThis study developed an 8-ERSRDEGs signature. Based on the expression of these genes, we constructed a diagnostic nomogram model in which agouti-related neuropeptide had a significantly greater impact on the model. The area under the curve values for the predictive value of the ERSRDEGs signature were 0.975 and 1.000 for GSE70866 and GSE110147, respectively. We developed a prognostic model based on the ERS scores of patients with IPF. Furthermore, we classified patients with IPF into two subtypes based on their signatures. The RT-qPCR validation results supported the reliability of most of our conclusions.ConclusionWe developed and verified a risk model using eight ERSRDEGs. These eight genes can potentially affect the progression of IPF by regulating ERS and immune responses.

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“…Indeed, the current data documents situations, including in primary epithelial cells, where there is synergy between the inflammatory stimulus and glucocorticoids on the induction of BIRC3 expression. Such observations may account for the presence of BIRC3 expression in severe asthma and the existence of BIRC3 polymorphisms that associate with asthma therefore warrant further investigation [ 26 , 71 ]. Mechanistically, BIRC3 expression was independently induced by glucocorticoids acting via the GR.…”

Section: Discussionmentioning

confidence: 99%

“…As signaling from many PRRs converges on NF-κB, it is perhaps not surprising that polymorphisms in BIRC3 have been associated with asthma [ 25 ]. In addition, BIRC3 expression correlates with markers of severe asthma [ 26 ], suggesting BIRC3 could contribute to a more prolonged, or more severe, inflammation. In contrast, BIRC3 may be protective in influenza virus infections and thus transcriptional induction of BIRC3 by inflammatory triggers may help protect from viral-induced cell death [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of BIRC2 and BIRC3 expression by inflammatory cytokines and glucocorticoids in pulmonary epithelial cells

et al. 2023

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Roles for the baculoviral inhibitor of apoptosis repeat-containing (BIRC) genes, BIRC2 and BIRC3, may include signaling to the inflammatory transcription factor, nuclear factor-κB (NF-κB) and protection from cell death. However, distinct functions for each BIRC are not well-delineated. Given roles for the epithelium in barrier function and host defence, BIRC2 and BIRC3 expression was characterized in pulmonary epithelial cell lines and primary human bronchial epithelial cells (pHBECs) grown as undifferentiated cells in submersion culture (SC) or as highly differentiated cells at air-liquid interface (ALI). In A549 cells, interleukin-1β (IL1B) and tumor necrosis factor α (TNF) induced BIRC3 mRNA (~20-50-fold), with maximal protein expression from 6–24 h. Similar effects occurred in BEAS-2B and Calu-3 cells, as well as SC and ALI pHBECs. BIRC2 protein was readily detected in unstimulated cells, but was not markedly modulated by IL1B or TNF. Glucocorticoids (dexamethasone, budesonide) modestly increased BIRC3 mRNA and protein, but showed little effect on BIRC2 expression. In A549 cells, BIRC3 mRNA induced by IL1B was unchanged by glucocorticoids and showed supra-additivity with TNF-plus-glucocorticoid. Supra-additivity was also evident for IL1B-plus-budesonide induced-BIRC3 in SC and ALI pHBECs. Using A549 cells, IL1B- and TNF-induced BIRC3 expression, and to a lesser extent, BIRC2, was prevented by NF-κB inhibition. Glucocorticoid-induced BIRC3 expression was prevented by silencing and antagonism of the glucocorticoid receptor. Whereas TNF, but not IL1B, induced degradation of basal BIRC2 and BIRC3 protein, IL1B- and TNF-induced BIRC3 protein remained stable. Differential regulation by cytokines and glucocorticoids shows BIRC2 protein expression to be consistent with roles in rapid signaling events, whereas cytokine-induced BIRC3 may be more important in later effects. While TNF-induced degradation of both BIRCs may restrict their activity, cytokine-enhanced BIRC3 expression could prime for its function. Finally, shielding from glucocorticoid repression, or further enhancement by glucocorticoid, may indicate a key protective role for BIRC3.

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Exploration of induced sputum BIRC3 levels and clinical implications in asthma

Cited by 8 publications

References 34 publications

Expression Analysis of BIRC3 as One Target Gene of Transcription Factor NF-κB for Esophageal Cancer

Expression Analysis of BIRC3 as One Target Gene of Transcription Factor NF-κB for Esophageal Cancer

Comprehensive analysis of an endoplasmic reticulum stress-related gene prediction model and immune infiltration in idiopathic pulmonary fibrosis

Differential regulation of BIRC2 and BIRC3 expression by inflammatory cytokines and glucocorticoids in pulmonary epithelial cells

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