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
;
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; 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.