Gene name: | FOXQ1 |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | 2BS |
Gene ID: | 94234 |
Category: | protein coding |
Phenotype: | Esophageal cancer |
Experimental category: | L |
PMID: | 28726780 |
Experiment: | DAPI staining//SA-β-gal activity assay//Flow cytometry |
Description: | Meanwhile, miR30-FOXQ1 also resulted in emerging the morphological features of senescence, characterized by enlarged and flattened cell size, increased senescenceassociated heterochromatin foci, elevated activity of senescence-associated β-galactosidase (SA-β-gal), a biomarker for senescent cells, and reduced S and increased G1 compartments compared with scramble control vector.Conversely, LPC-FOXQ1 induced much lower SA-β-gal activity and less cell cycle progression than the infection with its corresponding empty control vector. |
Target gene: | SIRT1//IL-6//IL-8//P16 |
Official symbol(s): | SIRT1//IL6//CXCL8//P16 |
R-AG-Target gene: | Upregulation//Downregulation//Downregulation//Downregulation |
Subcategory: | Binding to promoter |
Target gene experiment: | Western blot//qRT-PCR//CHIP-qPCR |
Target gene description: | Western blot analysis revealed that FOXQ1 overexpression significantly increased the protein level of SIRT1 in HEK293T cells.In parallel with the findings from western blot analysis, qRT-PCR analysis also showed a positive regulation of SIRT1 mRNA expression by FOXQ1,indicating that FOXQ1 could activate transcription of SIRT1.The ChIP-qPCR results indicated a significant enrichment of FOXQ1 in the promoter of SIRT1 in the FOXQ1 overexpressed cells compared with the control cells. LPC-FOXQ1 markedly decreased the mRNA abundance of IL-6 and IL-8 compared with control transfection . Besides, increased FOXQ1 expression resulted in a decreased level of p16INK4aprotein, while removal of FOXQ1 exhibited an opposite effect on p16INK4aprotein level. |
Regulatory pathway: | NF-κB |
R-AG-Pathway: | Upregulation |
Official symbol(s): | NFKB1 |
Pathway experiment: | Western blot |
Pathway description: | We found that the protein level of IκBα, an inhibitor of NF- κB, positively correlated with FOXQ1 and SIRT1.Western blot results revealed that the FOXQ1-induced upregulation of IκBα level was abolished by addition of EX-527 treatment.These results suggested that the FOXQ1-mediated regulation of SASP factors was dependent on SIRT1-NF-κB pathway. |
Annotation:
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