Effect and molecular mechanism of proteasome inhibitor in TRAIL-induced apoptosis resistance on malignant lymphoma cells
10.3760/cma.j.issn.1009-9921.2009.06.004
- VernacularTitle:蛋白酶体抑制剂在肿瘤坏死因子相对凋亡诱导配体诱导恶性淋巴瘤细胞凋亡抵抗中的作用及其分子机制
- Author:
Tiansuo ZHAO
;
Yurong SHI
;
He REN
;
Jihui HAO
- Publication Type:Journal Article
- Keywords:
TRAIL;
PS-341;
Lymphoma cells;
Apoptotic resistance
- From:
Journal of Leukemia & Lymphoma
2009;18(6):331-334
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect and molecular mechanism of proteasome inhibitor in TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis resistance on malignant lymphoma cells.Methods Raji cells were treated with TRAIL and proteasome inhibitor (PS-341) in vitro and the cell growth index was evaluated by MTT assay; cell cycle was analysed by flow cytometry; the protein and mRNA level of Bax were measured by Western blotting and real time RT-PCR. Results TRAIL inhibited proliferation of Raji cells at the concentration of 500 μg/L, but the inhibition rate was lower than that of the control cell:Hmy2.ciR.TRAIL arrested cell in G0/G1 phase. The Bax protein in Raji is degraded, but the Bax mRNA expression level does not change significantly .The effects of TRAIL was enhanced significantly 10 nmol/L PS-341 was added. Conclusion Raji cells are resistant in TRAIL-induced apoptosis. This effect may be related to the decrease of Bax protein. The Ubiquitin-proteasome pathway is involved in the degradation of Bax in TRAIL-treated Raji cells.