Relation between activation of NF-kappa B and chemotherapy induced apoptosis of leukemic cells.
- Author:
Xiao-ping XU
1
;
Jian-hui SHI
;
Lin LI
;
Zong-liang ZHANG
;
Wen-ying CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antineoplastic Agents, Phytogenic; pharmacology; Apoptosis; drug effects; In Situ Nick-End Labeling; Leukemia P388; drug therapy; pathology; Mice; NF-kappa B; antagonists & inhibitors; metabolism; Vincristine; pharmacology
- From: Chinese Journal of Oncology 2003;25(3):216-219
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo analyze the relation between activation of NF-kappa B and chemotherapy induced apoptosis of leukemic cells and the effect of vincristine (VCR) on them.
METHODSElectrophoretic mobility shift assay (EMSA) was used to detect the activation of NF-kappa B and tunel DNA electrophoresis was adopted to observe the apoptosis induced by cytosine arabinoside (Ara-C) and etopside (Vp-16) in P388 leukemic cells.
RESULTSThe activation of NF-kappa B induced by Ara-C and Vp-16 was obviously correlated to apoptosis in P388 cells. VCR (0.1 micromol/L) could suppress activation of NF-kappa B by 52% and 63% and significantly increase the apoptosis by 89% and 123% as induced by Ara-C (100 micromol/L) and Vp-16 (100 micromol/L). The activity of NF-kappa B could be found in P388 cells before being exposed to chemotherapeutic agent.
CONCLUSIONChemotherapeutic agents can induce apoptosis and activation of NF-kappa B of P388 cells. The mechanism of VCR potentiating chemotherapeutics induction of leukemia cell apoptosis may be related to its suppression of the NF-kappa B activity in the P388 cells.
