Aging Overview

Aging gene

Gene name: IFITM3
Aging type: Prevent
Aging characteristic:
Tissue type: Human OSCC primary tumour
Cell name: ORL-150,ORL-204
Gene ID: 10410
Category: protein coding
Phenotype: Oral cancer
Experimental category: L
PMID: 30949979
Experiment: SA-β-gal activity assay//Flow cytometry//Knockdown//Cell morphological analysis
Description: When examining cells that did not undergo cell death following IFITM3 knockdown, we noted that the cell morphology appeared to be flattened with an enlarged cytoplasm as well as an accumulation of vacuoles. This significant increase in senescence-associated βgalactosidase staining indicates that IFITM3 knockdown induces senescence in ORL-150 (48%) and ORL-204 (14.2%) cells compared to the respective NT control cells.By doing so, we indeed observed a significant increase of cells in the G1 phase following IFITM3 knockdown in ORL-150 (86.7%) and ORL-204 (62.5%) cells compared to NT control cells, thus confirming that IFITM3 knockdown induces senescence and accumulation of cells in the G1 cell cycle phase.


Regulatory relationship

Regulatory pathway: CCND1-CDK4-PRB
R-AG-Pathway: Upregulation
Official symbol(s): Regulation of retinoblastoma protein
Pathway experiment: Western blot//Knockdown
Pathway description: We found that the expression of CCND1 was markedly reduced following IFITM3 knockdown in both cell lines. Similarly, we found that the CDK4 expression levels were reduced, but recovered at day 6 post-transfection when IFITM3 levels increased again.The reductions in both CCND1 and CDK4 following IFITM3 knockdown eventually resulted in a reduction in RB phosphorylation (pRB) and to a lesser extent in total RB expression.


Aging network

Annotation:

The green line represents Upregulation.

The purple line represents Downregulation.

The orange line represents Activation.

The yellow line represents Inhibition.

The gray line represents Unclear.



Pathway view

About risk SNP and eQTL

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