Work

The tumor suppressor p33ING1benhances taxol-induced apoptosis by p53-dependent pathway in human osteosarcoma U2OS cells

Year: 2005

Type: article

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.

Source: Cancer Biology & Therapy

DOI: 10.4161/cbt.4.1.1372

Authors: Jin-Jun Zhu, Fo-Bao Li, Jun-Min Zhou, Zong-Chao Liu, Xiao-Feng Zhu, Wei-Ming Liao

Institutions: Sun Yat-sen University, The First Affiliated Hospital, Sun Yat-sen University, State Key Laboratory of Oncology in South China

Language: English

Topic: Cancer-related Molecular Pathways

Subfield: Oncology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: bronze

Funder: National Natural Science Foundation of China