| External factors: | Hepatocyte growth factor |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Ovarian cancer |
| Experiment: | SA-β-gal activity assay//Cell proliferation assay |
| Description: | The experiments showed that CM collected from OVCAR-3, SKOV-3, and A2780 cells inhibited proliferation of HPMCs in short-term conditions and reduced the number of divisions completed by those cells (CPD) before reaching senescence upon their prolonged exposure . These anti-proliferative effects of cancer cell-derived CM co.ncided with the induction of SA-β-Gal and the activation of DNA damage response, as evidenced according to increased incidence of DNA damage foci, i.e. γ-H2A.X and 53BP1.The study showed that HGF increased the expression of SA-β-Gal in a dosedependent manner and that the pre-incubation of CM with a specific anti-HGF antibody prevented its capability to up-regulate the enzyme. |
| Regulatory pathway: | P38 MAPK//Akt//NF-κB |
| R-EF-Pathway: | Activation//Activation//Activation |
| Official symbol(s): | MAPK14//AKT1//NFKB1 |
| Pathway experiment: | ELISA |
| Pathway description: | It has been found that CM from either OVCAR-3 or SKOV-3 cells activated AKT, JNK, NF-κB, and p38 MAPK, whereas CM from A2780 cells activated NF-κB and p38 MAPK. |
Annotation: