Table 2.
Presence of the cellular senescence phenotype offers therapeutic opportunities.
Characteristic | Synthetic lethal targeting of senescent cells |
---|---|
Cell morphology | |
SA-β-gal positive | |
Enlarged cell with prominent nuclei and cytoplasmic granularity | |
Metabolic alterations | |
Hypermetabolic | Glucose transport inhibitors phloretin, cytochalasin B, 2-deoxy-d-glucose [36] |
Glycolysis | AMPK inhibitor compound C [36]/AMPK activator and mTOR inhibitor metformin [50], [51] |
High protein turnover | Lysosomal V-ATPase inhibitors bafilomycin A1 and concanamycin A [36] |
Secretory phenotype | |
Pro-inflammatory cytokines | Tumor microenvironment cancer-based immunotherapy [52] |
Growth factors | Growth factor and growth factor receptor inhibitors (e.g. VEGF, IGF-1 inhibitors) [53] |
AMPK, adenosine monophosphate-activated protein kinase; ATPase, adenosine triphosphatase; IGF-1, insulin-like growth factor 1; mTOR, mammalian target of rapamycin; SA-β-gal, senescence-associated β-galactosidas; VEGF, vascular endothelial growth factor.