| Gene name: | PTEN |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | LN-18,U87,U251,U373,LN428 |
| Experiment: | Cell morphological analysis//SA-β-gal activity assay//Western blot |
| Description: | We first examined relative cell numbers and cellular morphologies, and observed that all cell types had decreased cell numbers in a dose-dependent manner following IR .Furthermore, microscopic analyses indicated that U87, U251, and U373 cells were positive for senescence-associated β-galactosidase (SA-β-Gal), a hall-mark of senescence, and for senescent morphology (large flattened shape).Cyclin-dependent kinase inhibitor p21, one of senescence markers, was dramatically increased in PTEN-deficient U87, U251, and U373 cells, but not in PTEN-proficient LN18 and LN428 cells, and cleaved poly (ADP-ribose) polymerase (PARP), which is an indicator of the biochemical changes due to caspase activation during apoptosis was detected only in LN18 and LN428 cells . |
| Regulatory pathway: | AKT-ROS-P53-P21 |
| R-AG-Pathway: | -- |
| Official symbol(s): | AKT1-ROS1-TP53-CDKN1A |
| Pathway experiment: | Western blot//SA-β-gal activity assay//Flow cytometry |
| Pathway description: | U87 cells were characterized by gradual increases in phospho-AKT, wt p53, and p21. AKT depletion also shifted cells from premature senescence to apoptosis as a response to IR , as observed in wt PTEN-expressing cells. AKT depletion resulted in decreases in both SA-β-Gal activity and intracellular ROS levels.In p53siRNA transfected cells before IR exposure, p21 expression was not induced , and cells showed decreased SA-β-Gal activity. Cells transfected with p21 siRNA before IR exposure showed phenotypes similar to those transfected with p53 siRNA. |
Annotation:
Loading,please wait...