Effect of Emodin Derivative E11 on T Lymphocytic Leukemia Cell Line Molt-4 and Its Possible Mechanisms.
- Author:
Yu-Ling HUANG
1
;
Wen-Feng WANG
2
;
Jian-Da HU
1
;
Jun-Ting ZHENG
1
;
Jing LI
1
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Caspase 3; metabolism; Caspase 9; metabolism; Cell Line, Tumor; drug effects; Cell Proliferation; Down-Regulation; Emodin; pharmacology; Humans; Leukemia, T-Cell; pathology; MAP Kinase Signaling System; Phosphatidylinositol 3-Kinases; metabolism; Poly(ADP-ribose) Polymerases; metabolism; Proto-Oncogene Proteins c-akt; metabolism; TOR Serine-Threonine Kinases; metabolism
- From: Journal of Experimental Hematology 2016;24(1):8-13
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of a new emodin derivative E11 on proliferation and apoptosis of T lymphocytic leukemia cell line Molt-4 and its possible mechanisms.
METHODSMTT method was used to plot cell growth curve. Colony culture assay was performed for studying the effect of emodin derivative E11 on colony-formation of Molt-4. The fluorescent microscopy with DAPI staining was used to examine the cell morphological changes after E11 treatment. DNA fragmentation method was used to detect the inducing effect of emodin derivative E11 on cell apoptosis. Western blot was used to determine the expressions of apoptosis-related proteins including procaspase-9, procaspase-3, PARP and PI3K/AKT, MAPK signalling pathway.
RESULTSEmodin derivative E11 could strongly inhibit the growth of Molt-4 with the IC50 in 48 h at 1.381 ± 0.1552 µmol/L in dose-dependent manner. 0.1 µmol/L of E11 could inhibit cell colony formation. The typrical apopototic morphologic changes of Molt cells treated with E11 could be observed under fluorescence microscope with DAPI staining. DNA apoptotic ladder could be observed by DNA fragmentation.The expressions of procaspase -9, procaspase-3, PARP, p-MAPK, p-AKT, mTOR, p-mTOR, p-P70 and p-4BEP1 were down-regulated, while expressions of MAPK, AKT, 4EBP1 and P70 were not changed remarkably after Molt-4 were treated with E11 for 48 h.
CONCLUSIONE11 can remarkably inhibit the proliferation and induce the apoptosis of Molt-4 cells. The mechanism of apoptosis of Molt-4 cells may be related with the suppression of PI3K/AKT and MAPK signalling pathways.
