CDX2 inhibits invasion and migration of gastric cancer cells by phosphatase and tensin homologue deleted from chromosome 10/Akt signaling pathway.
- Author:
Yong-Qiang LIU
;
Zhi-Gang BAI
;
Xue-Mei MA
;
Zhong-Tao ZHANG
1
Author Information
- Publication Type:Journal Article
- MeSH: CDX2 Transcription Factor; Cell Line, Tumor; Cell Movement; genetics; physiology; Chromosomes, Human, Pair 10; genetics; Epithelial-Mesenchymal Transition; genetics; physiology; Homeodomain Proteins; genetics; metabolism; Humans; Microfilament Proteins; genetics; metabolism; PTEN Phosphohydrolase; genetics; Phosphoric Monoester Hydrolases; genetics; metabolism; Proto-Oncogene Proteins c-akt; genetics; metabolism; Signal Transduction; genetics; physiology; Stomach Neoplasms; genetics; metabolism; pathology; Tensins; Wound Healing; genetics; physiology
- From: Chinese Medical Journal 2015;128(8):1065-1071
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDGastric cancer (GC) is one of the most prevalent malignancies in the world today, with a high mortality rate. CDX2 is a Drosophila caudal-related homeobox transcription factor that plays an important role in GC. Phosphatase and tensin homologue deleted from chromosome 10 (PTEN) is an important tumor suppressor which is widely expressed in normal human tissues. The aim of the study was to determine the relationship and mechanism between CDX2 and PTEN in invasion and migration of GC cells.
METHODSpcDNA3-CDX2 plasmids were transfected into MGC-803 cells to up-regulate CDX2 protein, and small interfering RNA-CDX2 was transfected to down-regulate CDX2. The influence of CDX2 or PTEN on cell migration and invasion was measured by invasion, migration and wound healing assays. Western blotting assay and immunofluorescence were used to detect the expression of CDX2, PTEN, phosphorylation of Akt, E-cadherin and N-cadherin. Statistical significance was determined by one-way analysis of variance.
RESULTSThe results showed that CDX2 reduced the migration and invasion of GC cells (P < 0.05), and inhibited the activity of Akt through down-regulating PTEN expression (P < 0.05). CDX2 also restrained epithelial-mesenchymal transition of GC cells.
CONCLUSIONSCDX2 inhibited invasion and migration of GC cells by PTEN/Akt signaling pathway, and that may be used for potential therapeutic target.
