The tumor suppressor p33ING1b enhances taxol-induced apoptosis by p53-dependent pathway in human osteosarcoma U2OS cells
| Autor: | Zong Chao Liu, Wei Ming Liao, Xiao Feng Zhu, Junmin Zhou, Jin Jun Zhu, Fo Bao Li |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Cancer Research
Cell cycle checkpoint DNA Repair Paclitaxel DNA repair Apoptosis Bone Neoplasms Cell Cycle Proteins chemistry.chemical_compound Downregulation and upregulation medicine Tumor Cells Cultured Humans Genes Tumor Suppressor Pharmacology Osteosarcoma Cell growth Chemistry Tumor Suppressor Proteins Cell Cycle Intracellular Signaling Peptides and Proteins Nuclear Proteins medicine.disease Genes p53 Antineoplastic Agents Phytogenic Growth Inhibitors Cell biology DNA-Binding Proteins Oncology Cancer research Molecular Medicine Ectopic expression Growth inhibition Inhibitor of Growth Protein 1 |
| Zdroj: | Cancer biologytherapy. 4(1) |
| ISSN: | 1538-4047 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|