GPI-PLD inhibits the growth of hepatoma cells by down-regulation of PI3K-Akt signaling pathway.
10.11817/j.issn.1672-7347.2014.09.001
- Author:
Zhiying YANG
1
,
2
;
Chaochao TAN
;
Zhiping YANG
;
He HUANG
;
Jianhua TANG
Author Information
1. Department of Human Anatomy and Histology,School of Basic Medical Science, Central South University, Changsha 410013
2. Department of Pharmacy, Changsha Health Vocational College, Changhsha 410100, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Carcinoma, Hepatocellular;
metabolism;
pathology;
Cell Line;
Down-Regulation;
Hep G2 Cells;
Humans;
Liver Neoplasms;
metabolism;
pathology;
Mice;
Mice, Nude;
Phosphatidylinositol 3-Kinases;
Phospholipase D;
metabolism;
Proto-Oncogene Proteins c-akt;
metabolism;
Signal Transduction;
Transfection
- From:
Journal of Central South University(Medical Sciences)
2014;39(9):873-878
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To clarify the effect of glycosylphosphatidylinositol-specific phospholipase D (GPIPLD) on hepatoma cells HepG2 and the possible molecular mechanism.
METHODS:MTT, fluorescent staining and Western blot were applied to analyze the effect and molecular mechanism of GPI-PLD on hepatoma cells by transfected high expression GPI-PLD model. We inoculated HepG2 in nude mice models to further clarify the effect of GPI-PLD on hepatoma cells in vivo.
RESULTS:Compared with the control groups, PI3K-Akt signaling pathway activity and proliferation of hepatoma cells were significantly inhibited in the GPI-PLD group. Nude mice models showed that the tumor growth and tumor weight [(1.87 ± 0.09) g] of the GPI-PLD group were significantly less than those of the blank control group [(2.20 ± 0.17) g] and the negative control group [(2.15 ± 0.09) g]. AST, ALT and AFP serum concentration in the GPI-PLD group were significantly lower than those of the control groups (P<0.05).
CONCLUSION:GPI-PLD can inhibit the proliferation of hepatoma cells and growth in vivo, and promote the apoptosis of hepatoma cells by reducing the activity of PI3K-Akt signaling pathway.
