The p33ING1b tumor suppressor cooperates with p53 to induce apoptosis in response to etoposide in human osteosarcoma cells.
Life Sci
; 78(13): 1469-77, 2006 Feb 23.
Article
in En
| MEDLINE
| ID: mdl-16325212
ABSTRACT
p33ING1b induces cell cycle arrest and stimulates DNA repair, apoptosis and chemosensitivity. The magnitude of some p33ING1b effects may be due to activation of the tumor suppressor p53. To investigate if the p33ING1b protein affected chemosensitivity of osteosarcoma cells, we overexpressed p33ING1b in p53+/+ U2OS cells or in p53-mutant MG63 cells, and then assessed for growth arrest and apoptosis after treatment with etoposide. p33ING1b increased etoposide-induced growth inhibition and apoptosis to a much greater degree in p53+/+ U2OS cells than in p53-mutant MG63 cells. Moreover, ectopic expression of p33ING1b markedly upregulated p53, p21WAF1 and bax protein levels and activated caspase-3 protein kinase in etoposide-treated U2OS cells. Together, our data indicate that p33ING1b prominently enhances etoposide-induced apoptosis through p53-dependent pathways in human osteosarcoma cells. p33ING1b may be an important marker and/or therapeutic target in the prevention and treatment of metastatic osteosarcoma.
Search on Google
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Nuclear Proteins
/
Tumor Suppressor Protein p53
/
Apoptosis
/
Tumor Suppressor Proteins
/
Intracellular Signaling Peptides and Proteins
/
Etoposide
Limits:
Humans
Language:
En
Journal:
Life Sci
Year:
2006
Document type:
Article
Affiliation country:
China