The tumor suppressor p33ING1b enhances taxol-induced apoptosis by p53-dependent pathway in human osteosarcoma U2OS cells.
Cancer Biol Ther
; 4(1): 39-47, 2005 Jan.
Article
in En
| MEDLINE
| ID: mdl-15662138
ABSTRACT
p33ING1b can stimulate cell cycle arrest, DNA repair, apoptosis and chemosensitivity. The actions of p33ING1b involve p53-dependent and p53-independent mechanisms. To investigate if the p33ING1b isoform is involved in the chemosensitivity of osteosarcoma cells, p33ING1b was overexpressed in p53+/+ U2OS cells or p53-mutant MG63 cells, and then cell growth arrest and apoptosis were assessed after treatment with taxol. The results showed that p33ING1b markedly increased taxol-induced growth inhibition and apoptosis in p53+/+ U2OS cells, but not in p53-mutant MG63 cells. Moreover, ectopic expression of p33ING1b could obviously upregulate p53, p21WAF1 and bax protein levels and activate caspase-3 in taxol-treated U2OS cells. Taken together, our data demonstrate that p33ING1b enhances taxol-induced apoptosis through p53-dependent pathway in human osteosarcoma cells. p33ING1b may be an important marker and/or therapeutic target in the prevention and treatment of osteosarcoma.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Bone Neoplasms
/
Osteosarcoma
/
Genes, p53
/
Paclitaxel
/
Cell Cycle Proteins
/
DNA-Binding Proteins
/
Growth Inhibitors
/
Antineoplastic Agents, Phytogenic
Limits:
Humans
Language:
En
Journal:
Cancer Biol Ther
Journal subject:
NEOPLASIAS
/
TERAPEUTICA
Year:
2005
Document type:
Article
Affiliation country:
China