The effects of Mcl-1 gene on ATRA-resistant HL-60 cell.
- Author:
Jin-rong FU
1
;
Wen-li LIU
;
Jian-feng ZHOU
;
Han-ying SUN
;
Miao ZHENG
;
Mei HUANG
;
Chun-rui LI
;
Dan RAN
;
Li LUO
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; genetics; Cell Differentiation; drug effects; genetics; Cell Proliferation; drug effects; Drug Resistance, Neoplasm; genetics; HL-60 Cells; drug effects; metabolism; Humans; Proto-Oncogene Proteins c-bcl-2; genetics; metabolism; RNA, Small Interfering; Tretinoin; pharmacology
- From: Chinese Journal of Hematology 2005;26(6):352-354
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of Mcl-1 gene in resistance of all-trans retinoic acid (ATRA) of leukemia cells.
METHODSLong-term, intermittent and repetitive exposure of HL-60 cells to ATRA was used to establish a multidrug-resistance cell line (HL-60/ATRA). HL-60/ATRA cells were transfected with Mcl-1 small interference RNA (siRNA) by Lipofectamine 2000. Western blot was used to detect the expression of Mcl-1. The proliferation, apoptosis and differentiation were evaluated by MTT assay, in situ nick end-labeling (TUNEL) and NBT assay, respectively.
RESULTSThe HL-60/ATRA could keep its undifferentiated and proliferative status to a high concentration of ATRA (100 nmol/L) with highly expressed Mcl-1 protein (relative grey scale 0.624 +/- 0.127). Mcl-1 gene knockdown by siRNA (relative grey scale 0.267 +/- 0.086) could reverse the resistance of ATRA of HL-60/ATRA by inhibiting proliferation, and inducing differentiation and apoptosis [apoptosis rate (18.5 +/- 4.5)%].
CONCLUSIONMcl-1 gene might be involved in ATRA resistance in HL-60 cells and inhibiting its expression could be a new approach to ATRA resistance reversion.
