The E2F transcription factor 2: What do we know?

Li, Luwen; Wang, Shiguan; Zhang, Yihang; Pan, Jihong

doi:10.5582/bst.2021.01072

Cited by 16 publications

(13 citation statements)

References 79 publications

(59 reference statements)

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“…The motif can be bound by E2F-related factors, Ets-related factors, MECP2 , IRF , RUNX3 , and OLIG2 ( Supplementary Figure 3 ). E2F -related factors, including TFDP1 , E2F6 , E2F7 , E2F1 , E2F4 , and E2F3 , are crucial for the cell cycle, cell fate, and cell differentiation, including those of neutrophils ( 26 , 27 ). In summary, DMSs would modulate the motif binding of several TFs and thus be involved in cellular biological processes during the accumulation of neutrophils in Munro’s microabscess.…”

Section: Resultsmentioning

confidence: 99%

Genome-wide DNA methylation of Munro’s microabscess reveals the epigenetic regulation in the pathogenesis of psoriasis

Zhang

Pan

et al. 2022

Front. Immunol.

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IntroductionMunro's microabscess is a typical pathological feature in the early psoriatic lesion, mainly characterized by the accumulation of neutrophils in the epidermis. DNA methylation microenvironment of Munro's microabscess and the crosstalk with transcription and its effect on neutrophils have not yet been revealed.MethodsPerformed genome-wide DNA methylation analysis and further differential methylation analysis of psoriatic skin lesions with and without Munro's microabscess from two batch samples consisting of 114 former samples in the discovery stage and 21 newly-collected samples in the validation stage. Utilized GO, MEME, and other tools to conduct downstream analysis on differentially methylated sites (DMSs). Correlation analysis of methylation level and transcriptome data was also conducted.ResultsWe observed 647 overlapping DMSs associated with Munro's microabscess. Subsequently, GO pathway analysis revealed that DNA methylation might affect the physical properties associated with skin cells through focal adhesion and cellsubstrate junction and was likely to recruit neutrophils in the epidermis. Via the MEME tool, used to investigate the possible binding transcription factors (TFs) of 20 motifs around the 647 DMSs, it was found that DNA methylation regulated the binding of AP1 family members and the recruitment of neutrophils in the epidermis through the TGF-beta pathway and the TH17 pathway. Meanwhile, combined with our earlier transcriptome data, we found DNA methylation would regulate the expressions of CFDP, SIRT6, SMG6, TRAPPC9, HSD17B7, and KIAA0415, indicating these genes would potentially promote the process of Munro's microabscess.DiscussionIn conclusion, DNA methylation may affect the course of psoriasis by regulating the progression of Munro's microabscess in psoriatic skin lesions.

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Section: Resultsmentioning

confidence: 99%

Genome-wide DNA methylation of Munro’s microabscess reveals the epigenetic regulation in the pathogenesis of psoriasis

Zhang

Pan

et al. 2022

Front. Immunol.

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“…It is known that E2F2 play a significant role in promoting the cell cycle [ 8 ]. Some studies demonstrate increased E2F2 gene expression in cancers such as ovarian cancer, non-small cell lung cancer, hepatocellular carcinoma and breast cancer [ 35 , 36 , 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…E2F2 belongs to the E2F family of transcription factors and it can bind to a Rb protein. It is known that the RB/E2F signalling pathway is associated with an important proliferation control at the G1/S checkpoint [ 8 ]. LTF encode lactotransferrin.…”

Section: Introductionmentioning

confidence: 99%

Expression Profiles of CDKN2A, MDM2, E2F2 and LTF Genes in Oral Squamous Cell Carcinoma

et al. 2022

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Background: Oral squamous cell carcinoma (OSCC) is one of the most commonly detected neoplasms worldwide. Not all mechanisms associated with cell cycle disturbances are known in OSCC. Examples of genes involved in the control of the cell cycle are CDKN2A, MDM2, E2F2 and LTF. The aim of this study was to examine the possible association between CDKN2A, MDM2, E2F2 and LTF mRNA expression and influence on clinical variables. Methods: The study group consisted of 88 Polish patients. The gene expression levels were assessed by quantitative reverse transcription PCR. Results: We found no statistically significant differences in the expression level of CDKN2A, MDM2, E2F2 and LTF genes in tumour samples compared to margin samples. No association was found between the gene expression levels and clinical parameters, except E2F2. The patients with G2 tumours had a significantly higher gene expression level of E2F2 than patients with low-grade G1 tumours. Conclusions: We have not demonstrated that a change in expression profiles of genes has a significant impact on the pathogenesis of OSCC. It may also be useful to conduct further studies on the use of E2F2 expression profile changes as a factor to describe the invasiveness and dynamics of OSCC development.

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“…The available evidence shows that E2F2 is controlled by cyclin-dependent kinases and their inhibitors. However, E2F2 induces the expression of cell cycle protein such as CCNA2 but does not increase the P21 level [ 34 , 35 ]. The previous report indicates that P21 expression may not be necessary for human fibroblasts senescence [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Alteration of E2F2 Expression in Governing Endothelial Cell Senescence

Liu

Chen

Xiao

et al. 2022

Genes

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Endothelial cell senescence has a vital implication for vascular dysfunction, leading to age-related cardiovascular disease, especially hypertension and atherosclerosis. E2F transcription factor 2 (E2F2) plays a critical role in cell proliferation, differentiation, and DNA damage response. Up to date, no study has ever connected E2F2 to vascular endothelial cell senescence. Here, we demonstrate that E2F2 is involved in endothelial cellular senescence. We found that E2F2 expression is decreased during the replicative senescence of human umbilical vein endothelial cells (HUVECs) and the aortas of aged mice. The knockdown of E2F2 in young HUVECs induces premature senescence characterized by an increase in senescence-associated β-galactosidase (SA-β-gal) activity, a reduction in phosphorylated endothelial nitric oxide synthase (p-eNOS) and sirtuin 1 (SIRT1), and the upregulation of senescence-associated secretory phenotype (SASP) IL-6 and IL-8. The lack of E2F2 promoted cell cycle arrest, DNA damage, and cell proliferation inhibition. Conversely, E2F2 overexpression reversed the senescence phenotype and enhanced the cellular function in the senescent cells. Furthermore, E2F2 deficiency downregulated downstream target genes including CNNA2, CDK1, and FOXM1, and overexpression restored the expression of these genes. Our findings demonstrate that E2F2 plays an indispensable role in endothelial cell senescence.

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The E2F transcription factor 2: What do we know?

Cited by 16 publications

References 79 publications

Genome-wide DNA methylation of Munro’s microabscess reveals the epigenetic regulation in the pathogenesis of psoriasis

Genome-wide DNA methylation of Munro’s microabscess reveals the epigenetic regulation in the pathogenesis of psoriasis

Expression Profiles of CDKN2A, MDM2, E2F2 and LTF Genes in Oral Squamous Cell Carcinoma

Alteration of E2F2 Expression in Governing Endothelial Cell Senescence

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