Inflammation-induced colon cancer in uPA-deficient mice is associated with a deregulated expression of Notch signaling pathway components

Afaloniati, Hara; Karagiannis, George S.; Karavanis, Emmanouel; Psarra, Theophano A.; Karampatzakis-Kouritas, Anastasios; Poutahidis, Theofilos; Angelopoulou, Katerina

doi:10.1007/s11010-019-03659-9

Cited by 4 publications

(4 citation statements)

References 49 publications

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“…Among the 165 DMRs, the most significant differences in methylation mapped to genes associated with diverse atopic diseases including AD, [44][45][46][47] asthma, [48][49][50][51][52] atopy in general, 53 and inflammatory responses. [54][55][56][57][58][59][60][61][62][63][64] In addition to maternal atopy, the risk of disease susceptibility was further enhanced when DMRs were included in risk modeling methyl donor intake and its potential effects on DNA methylation as a risk factor for atopy, [8][9][10] this did not appear relevant in our study as folate levels and vitamin B12 were comparable in pregnant mothers and independent of their atopy status.…”

Section: Discussionmentioning

confidence: 71%

“…To characterize molecular mechanisms including changes in methylation to explain the increased manifestations of atopic disease in children born to atopic mothers, we identified DMRs that distinguished atopic from non‐atopic mothers. Among the 165 DMRs, the most significant differences in methylation mapped to genes associated with diverse atopic diseases including AD, 44–47 asthma, 48–52 atopy in general, 53 and inflammatory responses 54–64 …”

Section: Discussionmentioning

confidence: 99%

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Molecular networks in atopic mothers impact the risk of infant atopy

Schedel

Leach

Strand

et al. 2022

Allergy

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Background:The prevalence of atopic diseases has increased with atopic dermatitis (AD) as the earliest manifestation. We assessed if molecular risk factors in atopic mothers influence their infants' susceptibility to an atopic disease. Methods: Pregnant women and their infants with (n = 174, high-risk) or without (n = 126, low-risk) parental atopy were enrolled in a prospective birth cohort. Global differentially methylated regions (DMRs) were determined in atopic (n = 92) and non-atopic | 245 SCHEDEL et al.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Molecular networks in atopic mothers impact the risk of infant atopy

Schedel

Leach

Strand

et al. 2022

Allergy

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“…NOTCH1 to 4 are transmembrane receptors that determine cell fate. The NOTCH Receptor 2 (NOTCH2) has been reported to exert distinct functions in regulating tissue homeostasis and cell fate determination ( Baron, 2017 ; Afaloniati et al, 2020 ). In infectious diseases, NOTCH2 is possibly involved in regulating the Epstein–Barr virus latent/lytic status ( Giunco et al, 2015 ), and 4.3% of hepatitis C virus-positive cells diffuse large B-cell lymphoma have NOTCH2 mutations ( Arcaini et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

CircDDX17 enhances coxsackievirus B3 replication through regulating miR-1248/NOTCH receptor 2 axis

Liu

Chen

et al. 2022

Front. Microbiol.

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Coxsackievirus B3 (CVB3) was one of the most common pathogens to cause viral myocarditis. Circular RNAs as novel non-coding RNAs with a closed loop molecular structure have been confirmed to be involved in virus infectious diseases, but the function in CVB3 infection was not systematically studied. In this study, we identified that hsa_circ_0063331 (circDDX17) was drastically decreased after CVB3 infection by circRNA microarray. In vivo and in vitro, when cells or mice were infected with CVB3, the expression of circDDX17 was significantly reduced, as demonstrated by quantitative real-time PCR assays. Additionally, circDDX17 enhanced CVB3 replication by downregulating the expression of miR-1248 in HeLa and HL-1 cells, and miR-1248 regulated CVB3 replication through interacting with the gene coding for NOTCH Receptor 2 (NOTCH2), and NOTCH2 could upregulate methyltransferase-like protein 3 (METTL3). Taken together, this study suggested that circDDX17 promoted CVB3 replication and regulated NOTCH2 by targeting miR-1248 as a miRNAs sponge.

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“…NOTCH1 to 4 are transmembrane receptors that determine cell fate. The NOTCH Receptor 2 (NOTCH2) has been reported to exert distinct functions in regulating tissue homeostasis and cell fate determination [15,16]. In infectious diseases, NOTCH2 is possibly involved in regulating the Epstein-Barr virus latent/lytic status [17], and 4.3% hepatitis C virus positive cells diffuse large B-cell lymphoma have NOTCH2 mutations [18].…”

Section: Introductionmentioning

confidence: 99%

CircDDX17 enhances CVB3 replication by N6-methyladenosine regulation through miR-1248/NOTCH2 targeting

Shen

Liu

et al. 2022

Preprint

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N6-methyladenosine (m6A) is the most prevalent internal mRNA modification in eukaryotes. m6A is necessary for RNA metabolism and function, and influences RNA viruses replication. Methyltransferase-like protein 3 (METTL3) is a “writer” to regulating m6A. Coxsackievirus B3 (CVB3), belonging to the genus Enterovirus of the Picornaviridae family, are species of non-enveloped, positive single-stranded RNA virus. CVB3 infection reduces circular RNA_DDX17 (circDDX17) expression level in HeLa and HL-1 cells, as in viral myocarditis (VM). CircDDX17 enhanced CVB3 replication in HeLa and HL-1 cells and regulated NOTCH Receptor 2 (NOTCH2) by targeting microRNA-1248 (miR-1248) as microRNAs (miRNAs) sponge. NOTCH2 interaction with METTL3, through m6A proteins like methyltransferase-like protein 14 (METTL14), AlkB Homolog 5 (ALKBH5), and YTH N6-Methyladenosine RNA Binding Protein 1 (YTHDF1) to improve CVB3 replication in host cells. Taken together, this study suggests that circDDX17 targets miR-1248 to regulate NOTCH2 expression and regulates METTL3 to enhance CVB3 replication in cells by m6A relation protein.

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Inflammation-induced colon cancer in uPA-deficient mice is associated with a deregulated expression of Notch signaling pathway components

Cited by 4 publications

References 49 publications

Molecular networks in atopic mothers impact the risk of infant atopy

Molecular networks in atopic mothers impact the risk of infant atopy

CircDDX17 enhances coxsackievirus B3 replication through regulating miR-1248/NOTCH receptor 2 axis

CircDDX17 enhances CVB3 replication by N6-methyladenosine regulation through miR-1248/NOTCH2 targeting

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