Regulation of <scp>CXCL</scp>1 chemokine and <scp>CSF</scp>3 cytokine levels in myometrial cells by the <scp>MAFF</scp> transcription factor

Saliba, James; Coutaud, Baptiste; Solovieva, Vera; Lu, Fangshi; Blank, Volker

doi:10.1111/jcmm.14136

Cited by 22 publications

(15 citation statements)

References 60 publications

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“…But the downstream signal moleculars of this pathway in HCC are still unclear. Previous researches indicated that MafF participated in oxidant stress response, inflammatory response, and cell motility by regulating the transcription of related genes such as heme oxygenase 1 (HO-1) and matrix metalloproteinases (MMPs) 9,35 . More studies need to be performed to elucidate the exact downstream moleculars of the circ-ITCH/miR-224-5p/MafF pathway in HCC, which will provide a new perspective for early diagnostic biomarkers and potential therapeutic targets of HCC.…”

Section: Discussionmentioning

confidence: 99%

MafF Is Regulated via the circ-ITCH/miR-224-5p Axis and Acts as a Tumor Suppressor in Hepatocellular Carcinoma

Deng

Zhong

et al. 2020

oncol res

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MafF is a member of the basic leucine zipper (bZIP) transcription factor Maf family and is commonly downregulated in multiple cancers. But the expression and function of MafF in hepatocellular carcinoma (HCC) remain unclear. In this study, we investigated the relationship between endogenous MafF expression and HCC progression and explored the regulatory mechanism of MafF expression in HCC. We found that MafF decreased in HCC tissues and cells. Lentivirus-mediated MafF overexpression inhibited HCC cell proliferation and induced cell apoptosis. Bioinformatics analysis and luciferase assay identified MafF as a direct target of miR-224-5p. RNA pull-down assay demonstrated that circular RNA circ-ITCH could sponge miR-224-5p specifically in HCC. The rescue experiments further elucidated that the expression and antitumor effects of MafF could be regulated via the circ-ITCH/miR-224-5p axis. This study verified that MafF acted as a tumor suppressor in HCC and revealed the upstream regulation mechanism of MafF, which provided a new perspective for potential therapeutic targets of HCC.

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Section: Discussionmentioning

confidence: 99%

MafF Is Regulated via the circ-ITCH/miR-224-5p Axis and Acts as a Tumor Suppressor in Hepatocellular Carcinoma

Deng

Zhong

et al. 2020

oncol res

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“…Moreover, WT1 has also been involved in cardiac development and disease(53-55), a link that was further supported by our phenome-wide association look-up results, since this region was associated with hypertension and cardiovascular disease (Supplementary Figure 3 and 4, Supplementary Tables 5 and 6). In this line, many associations we report point towards a link between metabolic and cardiovascular health and pelvic organ prolapse (KLF13, DUSP16, MAFF, VCL and LDAH), which was mirrored by positive genetic correlations with a range of cardiometabolic phenotypes (56)(57)(58)(59)(60)(61)(62)(63)(64)(65).…”

Section: Interpretation Of Findings and Comparison To Other Studiesmentioning

confidence: 91%

Advancing our understanding of genetic risk factors and potential personalized strategies in pelvic organ prolapse: largest GWAS to date reveals 19 novel associated loci

Pujol-Gualdo

Läll

Lepamets

et al. 2021

Preprint

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ObjectivesTo identify the genetic determinants of pelvic organ prolapse (POP) and assess the predictive ability of polygenic risk scores (PRS) alone or in combination with clinical risk factors.DesignMeta-analysis of genome-wide association studies (GWAS) and PRS construction and validation.SettingGWAS summary statistics from three European datasets and individual-level data from Estonian Biobank, including phenotype questionnaire and measurement panel, together with follow-up data from linkage with national health-related registries.ParticipantsA total of 28,086 women with POP and 546,321 controls of European ancestry. Genetic risk scores were derived from a dataset of 20,118 cases and 427,426 controls of European ancestry and validated in a target dataset of 7,896 cases and 118,895 controls. Cases were defined using ICD codes and classical risk factors were derived from questionnaire data and ICD10 codes.ResultsThe identified novel loci reinforce the role of connective tissue abnormalities, urogenital tract development and point towards association with a range of cardiometabolic traits. A novel PRS combining 3,242,959 variants demonstrated that women in the top 5% have 1.63 (95% CI: 1.37 to 1.93) times the hazard of developing POP compared to the rest of the women. When analyzing PRS in incident POP, it showed similar predictive ability (Harrell C-statistic 0.583, sd=0.007) than five established clinical risk factors (number of children, body mass index (BMI), ever smoked, constipation and asthma) combined (Harrell C-statistic 0.588, sd=0.007) and demonstrated its incremental value in combination with these (Harrell C-statistic 0.630, sd=0.007).ConclusionsThe largest GWAS meta-analysis in POP to date identified 26 genetic loci which establish links between POP and connective tissue abnormalities, urogenital development and cardiometabolic health. We present a PRS for POP which provides the first potential tool for preventive strategies and early detection of higher risk susceptibility to POP including genetic risk factors.

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“…In Pde6b rd10 mice, Maff was highly upregulated. The MAFF protein can regulate photoreceptor gene expression and is closely associated with inflammatory responses in neuronal diseases (Katsuoka et al, 2003;Chevillard et al, 2007;Saliba et al, 2019). We speculate that constant MAFF activation may contribute to inflammatory processes in the microenvironment through pro-inflammatory cytokines or chemokines, thereby mediating photoreceptor cell death.…”

Section: Roles Of Transcription Factors In Regulating Rdmentioning

confidence: 92%

RNA Biological Characteristics at the Peak of Cell Death in Different Hereditary Retinal Degeneration Mutants

Wei

Feng

et al. 2021

Front. Genet.

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Purpose: The present work investigated changes in the gene expression, molecular mechanisms, and pathogenesis of inherited retinal degeneration (RD) in three different disease models, to identify predictive biomarkers for their varied phenotypes and to provide a better scientific basis for their diagnosis, treatment, and prevention.Methods: Differentially expressed genes (DEGs) between retinal tissue from RD mouse models obtained during the photoreceptor cell death peak period (Pde6brd1 at post-natal (PN) day 13, Pde6brd10 at PN23, Prphrd2 at PN29) and retinal tissue from C3H wild-type mice were identified using Illumina high-throughput RNA-sequencing. Co-expression gene modules were identified using a combination of GO and KEGG enrichment analyses and gene co-expression network analysis. CircRNA-miRNA-mRNA network interactions were studied by genome-wide circRNA screening.Results:Pde6brd1, Pde6brd10, and Prphrd2 mice had 1,926, 3,096, and 375 DEGs, respectively. Genes related to ion channels, stress, inflammatory processes, tumor necrosis factor (TNF) production, and microglial cell activation were up-regulated, while genes related to endoplasmic reticulum regulation, metabolism, and homeostasis were down-regulated. Differential expression of transcription factors and non-coding RNAs generally implicated in other human diseases was detected (e.g., glaucoma, diabetic retinopathy, and inherited retinal degeneration). CircRNA-miRNA-mRNA network analysis indicated that these factors may be involved in photoreceptor cell death. Moreover, excessive cGMP accumulation causes photoreceptor cell death, and cGMP-related genes were generally affected by different pathogenic gene mutations.Conclusion: We screened genes and pathways related to photoreceptor cell death. Additionally, up-stream regulatory factors, such as transcription factors and non-coding RNA and their interaction networks were analyzed. Furthermore, RNAs involved in RD were functionally annotated. Overall, this study lays a foundation for future studies on photoreceptor cell death mechanisms.

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Regulation of CXCL1 chemokine and CSF3 cytokine levels in myometrial cells by the MAFF transcription factor

Cited by 22 publications

References 60 publications

MafF Is Regulated via the circ-ITCH/miR-224-5p Axis and Acts as a Tumor Suppressor in Hepatocellular Carcinoma

MafF Is Regulated via the circ-ITCH/miR-224-5p Axis and Acts as a Tumor Suppressor in Hepatocellular Carcinoma

Advancing our understanding of genetic risk factors and potential personalized strategies in pelvic organ prolapse: largest GWAS to date reveals 19 novel associated loci

RNA Biological Characteristics at the Peak of Cell Death in Different Hereditary Retinal Degeneration Mutants

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