Study of molecular mechanism of doxorubicin enhancement of TRAIL, inducing apoptosis of myeloma cell line KM3.
- Author:
Hua-fang WANG
1
;
Zhao-hui CHEN
;
Chun-yan SUN
;
Yu HU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Line, Tumor; Doxorubicin; pharmacology; Drug Interactions; Humans; Multiple Myeloma; metabolism; pathology; Receptors, TNF-Related Apoptosis-Inducing Ligand; genetics; metabolism; TNF-Related Apoptosis-Inducing Ligand; pharmacology; Transcription Factor RelA; genetics; metabolism
- From: Chinese Journal of Hematology 2007;28(1):30-32
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the molecular mechanism of doxorubicin enhancement of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) inducing apoptotic effect on multiple myeloma cell line KM3.
METHODSApoptosis was studied independently through flow cytometry analysis and TUNEL staining. The expression of death receptor 5 (DR5) and nuclear factor P65 in nuclear was examined by Western blot.
RESULTSThe apoptosis ratio of KM3 cells was 20.88%, 40.03%, 57.87%, 60.82% respectively when treated with different concentration of TRAIL (10, 20, 50, 100 ng/ml) combining with doxorubicin. It is markedly higher than the group treated with TRAIL or doxorubicin alone. DR5 expression increased while P65 decreased as the doses of doxorubicin increased when KM3 cells treated with doxorubicin (0.5, 1.0, 2.0 and 4.0 microg/ml) plus 20 ng/ml TRAIL.
CONCLUSIONIncreasing the expression of DR5 and nuclear transferring of P65 are the important molecular mechanism by which doxorubicin enhances TRAIL-inducing apoptosis of KM3 cells.
