| Gene name: | KCNJ12 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | PC-3,DU 145,LNCaP,MKN74,SNU638,SNU668,MCF-7,SK-BR-3,T47D |
| Experiment: | Cell morphological analysis//SA-β-gal activity assay//Knockdown//Western blot |
| Description: | Doxorubicin-treated PC-3 cells overexpressing Kir2.2 exhibited improved survival, decreased growth inhibition, and reduced accumulation of SA-β-Gal compared with doxorubicin-treated control PC-3 cells.All tested cancer cells from different tumor tissues, including prostate (PC-3, DU145, and LNCaP), stomach (MKN74, SNU638 and SNU668), and breast (MCF7, SK-BR3, and T47D),displayed cellular enlargement and flattening and were positive for SA-β-Gal staining following knockdown of Kir2.2, which lasted for up to 10 days .Previously reported senescence marker proteins,including PAI-1, osteonectin, and transglutaminase, were induced after Kir2.2 knockdown in the tested cancer cells. |
| Target gene: | P27 |
| Official symbol(s): | P27 |
| R-AG-Target gene: | -- |
| Subcategory: | Unclear |
| Target gene experiment: | Knockdown//Immunostaining//Western blot |
| Target gene description: | Kir2.2 knockdown induced ROS accumulation. Rescue of Kir2.2 levels by Kir2.2 overexpression restored intracellular ROS to levels comparable with those in controls, indicating that the accumulation of ROS was directly de pendent on the level of Kir2.2.p27 knockdown decreased ROS generation and the ROS scavenger NAC prevented p27 synthesis in PC-3 cells after transfection of siKir2.2. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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