Up-regulation of ErbB3-binding protein 1 inhibits the growth of esophageal carcinoma cells.
- Author:
Hao JIANG
1
;
Dong-Ping LIU
2
;
Dong XIE
2
;
Dong-Zhi WEI
3
Author Information
1. State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, China.
2. Institute of Nutrition Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
3. State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai 200237, China. dzhwei@ecust.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Carcinoma, Squamous Cell;
Cell Line, Tumor;
Cell Proliferation;
Down-Regulation;
Esophageal Neoplasms;
Humans;
Keratin-20;
Mice;
Mice, Nude;
Real-Time Polymerase Chain Reaction;
Transfection;
Up-Regulation
- From:
Acta Physiologica Sinica
2016;68(6):740-746
- CountryChina
- Language:Chinese
-
Abstract:
The objective of this study was to investigate the role of ErbB3-binding protein 1 (Ebp1) in the growth of esophageal squamous cell carcinoma (ESCC) cells and the underlying mechanism. Eca109 and KYSE150 cells were transfected with lentiviral vector carrying Ebp1 gene. The mRNA levels of Ebp1 in esophageal cancer tissues and paired adjacent normal tissues were examined by real-time PCR. The growth and viability of esophageal carcinoma cells were assessed using MTT and crystal violet assays, respectively. Clone-forming abilities of Eca109 and KYSE150 cells were analyzed by soft agar assay. Apoptotic rates of esophageal carcinoma cells were detected by flow cytometry, and expression levels of the proteins involved in apoptosis were assessed by Western blot. Tumorigenicity of Eca109 cells were detected by nude mouse transplantation tumor experiment. The results indicated that the mRNA levels of Ebp1 in esophageal cancer tissues was down-regulated compared with paired adjacent normal tissues. The growth and viability of Eca109 and KYSE150 cells were all suppressed by Ebp1 overexpression. Besides, Ebp1 overexpression induced apoptosis, increased Rb and P53 expressions, and decreased CyclinD1 expression in Eca109 and KYSE150 cells. In addition, Ebp1 overexpression inhibited the tumorigenesis of Eca109 cells in vivo. These results suggest that Ebp1 may suppress the growth of esophageal carcinoma cells in vitro and in vivo by inducing apoptosis.
