| 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 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. |
Annotation:
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