Association between E-cadherin and sensitivity of hepatocellular carcinoma to treatment with epidermal growth factor receptor tyrosine kinase inhibitor
10.3724/SP.J.1008.2014.00915
- Author:
Rong-Chun XING
1
Author Information
1. Department of General Surgery, The First Clinical Medicine College, Three Gorges University
- Publication Type:Journal Article
- Keywords:
E-cadherin;
Epidermal growth factor receptor;
Hepatocellular carcinoma;
Neoplasm drug resistance;
Tyrosine kinase inhibitor
- From:
Academic Journal of Second Military Medical University
2014;35(8):915-919
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of E-cadherin in resistance of hepatocellular carcinoma to treatment with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). Methods Four liver cancer cell lines were used in the present study, namely, HepG2, BEL-7404, SK-HEP-1 and MHCC97. E-cadherin protein expression in the four cell lines was examined by Western blotting analysis. MTT method was used to examine the relationship between E-cadherin expression and inhibition rates of liver cancer cells treated with EGFR-TKI. Results E-cadherin was positive in HepG2 and BEL-7404 cells, and they were sensitive to EGFR-TKI treatment; the survival rates of HepG2 and BEL-7404 cells were correlated with the concentrations of PD153035 and gefitinib (P<0.05). E-cadherin was negative in SK-HEP-1 and MHCC97 cells, and they were both resistant to EGFR-TKI treatment, and there was no association between SK-HEP-1 and MHCC97 cell survival rates and concentrations of PD153035 and gefitinib(P>0.05). The sensitivity of SK-HEP-1 cells to EGFR-TKI was significantly increased after transfected with E-cadherin compared with those transfected with empty vectors(P<0.05). Conclusion E-cadherin plays an important role in regulating the sensitivity of EGFR molecule targeted therapy.
