NIBAN1, Exploring its Roles in Cell Survival Under Stress Context

Diana, Paula; Carvalheira, Gianna

doi:10.3389/fcell.2022.867003

Cited by 11 publications

(11 citation statements)

References 72 publications

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“…Our findings are in accordance with existing knowledge, as recent studies also demonstrated significant enrichment of the IFN-I pathway and innate antiviral activity following secondary BNT162b2 immunization [ 15 , 16 ]. The 18 downregulated genes were found to be biologically unlinked, implying that their differential expression has little, if any, biological significance, as these genes are mostly involved in erythrocyte functions and metabolic pathways, such as activity of alkaline phosphatase, endoplasmic reticulum stress response and endothelial cell and neutrophil migration [ 17 , 18 , 19 , 20 , 21 ]. In contrast to Arunachalam et al, we were unable to identify any correlation between the innate transcriptional signatures and adaptive immune response or age, most probably due to the small size of our cohort [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 mRNA Dual Immunization Induces Innate Transcriptional Signatures, Establishes T-Cell Memory and Coordinates the Recall Response

et al. 2023

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Background: mRNA vaccines have played a crucial role in controlling the SARS-CoV-2 global pandemic. However, the immunological mechanisms involved in the induction, magnitude and longevity of mRNA-vaccine-induced protective immunity are still unclear. Methods: In our study, we used whole-RNA sequencing along with detailed immunophenotyping of antigen-specific T cells and humoral RBD-specific response to dual immunization with the Pfizer–BioNTech mRNA vaccine (BNT162b2) and correlated them with response to an additional dose, administered 10 months later, in order to comprehensively profile the immune response of healthy volunteers to BNT162b2. Results: Primary dual immunization induced upregulation of the Type I interferon pathway and generated spike protein (S)-specific IFN-γ+ and TNF-α+ CD4 T cells, S-specific memory CD4 T cells, and RBD-specific antibodies against SARS-CoV-2. S-specific CD4 T cells induced by the primary series correlated with the RBD-specific antibody titers to a third dose. Conclusions: This study demonstrates the induction of both innate and adaptive immunity in response to the BNT162b2 mRNA vaccine in a coordinated manner and identifies the central role of primarily induced CD4+ T cells as a predictive biomarker of the magnitude of anamnestic immune response.

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Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 mRNA Dual Immunization Induces Innate Transcriptional Signatures, Establishes T-Cell Memory and Coordinates the Recall Response

et al. 2023

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“…Multiple genes that were affected in this resulting list have been implicated to various cancer pathologies. This includes BNIP3 63 , HIST1H4L 64 , TBX3 65 (observed in all six treatments), early growth response factor 1 (EGR1) 66 , solute carrier family 7 member 11 (SLC7A11) 65 (observed in 5 treatments) niban apoptosis regulator 1 (NIBAN1) 67 and fos proto-oncogene (FOS) 68 (observed in 3 treatments). In addition, multiple PFAS-affected genes have previously been linked to neuronal health, including MANF 69 , TXNIP 70 (impacted in all six treatments), and tolloid-like protein 2 ( TLL2) 71 (impacted in 5 treatments).…”

Section: Resultsmentioning

confidence: 99%

“…Multiple genes that were affected in this resulting list have been implicated to various pathologies. These include BNIP3 57 , HIST1H4L 58 , TBX3 59 , MANF 60 and TXNIP 61 (observed in all six treatments), early growth response factor 1 ( EGR1 ) 62 , solute carrier family 7 member 11 ( SLC7A11 ) 59 and tolloid-like protein 2 ( TLL2 ) 63 (observed in 5 treatments), niban apoptosis regulator 1 ( NIBAN1 ) 64 and fos proto-oncogene ( FOS ) 65 (observed in 3 treatments). Importantly, MANF and TXNIP have previously been implicated in neuronal health.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomics effects of per- and polyfluorinated alkyl substances in differentiated neuronal cells

Running,

Karageorgiou,

Camdzic

et al. 2024

Preprint

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Per- and polyfluorinated alkyl substances (PFAS) are ubiquitous in most environments, accumulate in several tissues, and can adversely affect human health. PFAS have been implicated in neurodegenerative and behavioral disorders. However, the mechanisms through which PFAS accumulation in neurons affects biological function remain unknown. In this study, SH-SY5Y neuroblastoma cells were used to investigate how perfluorooctanoic acid (PFOA), perfluorooctansulfonic acid (PFOS), perfluorodecanoic acid (PFDA) perfluorodecanesulfonic acid (PFDS), 8:2 fluorotelomer sulfate (8:2 FTS) and 8:2 fluorotelomer alcohol (8:2 FTOH) exposures influence neuronal health. After a 30 microM-, 24-hour exposure, cells accumulated up to 800 ng PFAS/mg protein. Transcriptomics analysis of control and PFAS-exposed cells revealed 721 genes were differentially expressed across six treatments (padj < 0.05). Eleven of these differentially expressed genes were observed for all treatments, suggesting that these genes are potential markers for neuronal PFAS exposure. In PFOA-treated cells, we observed multiple downregulated genes are enriched for functions related to synaptic growth and neural function. In contrast, upregulated genes in PFOS, PFDS, FTS, and FTOH-treated cells showed enrichment in functions related to response to hypoxia and amino acid metabolism. Overall, our results highlight specific biological processes that potentially underlie negative effects of PFAS on neuronal health.

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“…The NIBAN1 (niban apoptosis regulator 1) gene, also known as FAM129A , belongs to the FAM129 family (family with sequence similarity 129), which has important cellular functions in a number of diseases and carcinogenic processes. 58 NIBAN1 plays a significant role in cellular homeostasis through the regulation of cell stress and autophagy. 35 , 58 , 59 In this study, we show that phenformin treatment strongly increased the expression of DDIT4 and NIBAN1 in OSCC cells in vivo and in vitro, and importantly, the knockdown of either DDIT4 or NIBAN1 suppressed the expression of autophagic markers induced by phenformin, which suggests that phenformin induces OSCC cell autophagy dependent on DDIT4 and NIBAN1 expression.…”

Section: Discussionmentioning

confidence: 99%

Phenformin activates ER stress to promote autophagic cell death via NIBAN1 and DDIT4 in oral squamous cell carcinoma independent of AMPK

Zhuang,

Wang,

Deng

et al. 2024

Int J Oral Sci

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The efficient clinical treatment of oral squamous cell carcinoma (OSCC) is still a challenge that demands the development of effective new drugs. Phenformin has been shown to produce more potent anti-tumor activities than metformin on different tumors, however, not much is known about the influence of phenformin on OSCC cells. We found that phenformin suppresses OSCC cell proliferation, and promotes OSCC cell autophagy and apoptosis to significantly inhibit OSCC cell growth both in vivo and in vitro. RNA-seq analysis revealed that autophagy pathways were the main targets of phenformin and identified two new targets DDIT4 (DNA damage inducible transcript 4) and NIBAN1 (niban apoptosis regulator 1). We found that phenformin significantly induces the expression of both DDIT4 and NIBAN1 to promote OSCC autophagy. Further, the enhanced expression of DDIT4 and NIBAN1 elicited by phenformin was not blocked by the knockdown of AMPK but was suppressed by the knockdown of transcription factor ATF4 (activation transcription factor 4), which was induced by phenformin treatment in OSCC cells. Mechanistically, these results revealed that phenformin triggers endoplasmic reticulum (ER) stress to activate PERK (protein kinase R-like ER kinase), which phosphorylates the transitional initial factor eIF2, and the increased phosphorylation of eIF2 leads to the increased translation of ATF4. In summary, we discovered that phenformin induces its new targets DDIT4 and especially NIBAN1 to promote autophagic and apoptotic cell death to suppress OSCC cell growth. Our study supports the potential clinical utility of phenformin for OSCC treatment in the future.

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NIBAN1, Exploring its Roles in Cell Survival Under Stress Context

Cited by 11 publications

References 72 publications

SARS-CoV-2 mRNA Dual Immunization Induces Innate Transcriptional Signatures, Establishes T-Cell Memory and Coordinates the Recall Response

SARS-CoV-2 mRNA Dual Immunization Induces Innate Transcriptional Signatures, Establishes T-Cell Memory and Coordinates the Recall Response

Transcriptomics effects of per- and polyfluorinated alkyl substances in differentiated neuronal cells

Phenformin activates ER stress to promote autophagic cell death via NIBAN1 and DDIT4 in oral squamous cell carcinoma independent of AMPK

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