期刊
BMC CANCER
卷 16, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/s12885-016-2252-y
关键词
Hepatocellular carcinoma; Epithelial cell adhesion molecule; Doxorubicin; 5-FU; Cisplatin
类别
资金
- American Diabetes Association Basic Science Award [1-13-BS-109]
Background: The low survival rate of hepatocellular carcinoma (HCC) is partly attributable to its resistance to existing chemotherapeutic agents. Until now, there have been limited chemotherapeutic agents for liver cancer. Epithelial cell adhesion molecule (EpCAM) has been found to be over-expressed during stages of carcinogenesis and has been associated with poor overall survival in many cancers. The aim of this study was to evaluate EpCAM expression in HCC and evaluate the effects of EpCAM to established chemotherapy. Methods: Three human hepatocellular carcinoma cell lines-HepG2, Hep3B and HuH-7-were pre- and post-treated with doxorubicin, 5-fluorouracil (5-FU) and cisplatin. Cell viability and EpCAM protein expression were measured by MTT assay and Western Blotting respectively. EpCAM positive cells were analyzed by flow cytometry. To evaluate the effects of doxorubicin efficacy on EpCAM positive cells, a small interfering RNA (siRNA) specific to EpCAM was transfected into the cells and treated with doxorubicin. Results: EpCAM was significantly down-regulated by doxorubicin treatment in all three HCC cell lines (P < 0.05 or 0.01). EpCAM expression was down-regulated by the 5-FU and cisplatin in HepG2 cells, however the EpCAM expression was up-regulated by 5-FU and cisplatin in Hep3B cell line. EpCAM expression was down-regulated by 5-FU, and up-regulated by cisplatin in Huh-7 cell line. Flow cytometry assay showed doxorubicin exposure decreased EpCAM positive cell quantities in three HCC cell lines. EpCAM siRNA knock-down attenuated cell mortality after doxorubicin exposure. Conclusion: All of these findings demonstrate that EpCAM is one of targets of chemoresistence.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据