Cancer Biol Ther 2005,
PMID: 15662138
Zhu, Jin-Jun; Li, Fo-Bao; Zhou, Jun-Min; Liu, Zong-Chao; Zhu, Xiao-Feng; Liao, Wei-Ming
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.
Diseases/Pathways annotated by Medline MESH: Bone Neoplasms, Osteosarcoma
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Text Mining Data
caspase-3 → p33ING1b: "
Moreover, ectopic expression of
p33ING1b could obviously upregulate p53, p21WAF1 and bax protein levels and
activate caspase-3 in taxol treated U2OS cells
"
caspase-3 → p33ING1b: "
Moreover, ectopic expression of p33ING1b could obviously upregulate p53, p21WAF1 and bax protein levels and activate caspase-3 in taxol treated U2OS cells
"
Manually curated Databases
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