Epithelial cell adhesion molecule in human hepatocellular carcinoma cell lines: a target of chemoresistence

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 stag...

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Bibliographic Details
Published in:BMC cancer 2016-03, Vol.16 (228), p.228-228, Article 228
Main Authors: Li, Yan, Farmer, Russell W, Yang, Yingbin, Martin, Robert C G
Format: Article
Language:English
Subjects:
Anthracyclines
Antibodies
Apoptosis
Cancer
Cancer therapies
Carcinoma, Hepatocellular - drug therapy
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - pathology
Care and treatment
Cell adhesion & migration
Cell cycle
Cell Survival - drug effects
Chemotherapy
Cisplatin - administration & dosage
Doxorubicin - administration & dosage
Drug Resistance, Neoplasm - genetics
Epithelial Cell Adhesion Molecule - biosynthesis
Epithelial Cell Adhesion Molecule - genetics
Flow cytometry
Fluorides
Fluorouracil - administration & dosage
Gene Expression Regulation, Neoplastic - drug effects
Health aspects
Hep G2 Cells
Hepatoma
Humans
Liver cancer
Liver Neoplasms - drug therapy
Liver Neoplasms - pathology
Metabolites
Patient outcomes
Penicillin
RNA, Small Interfering
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Summary: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. 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. EpCAM was significantly down-regulated by doxorubicin treatment in all three HCC cell lines (P
ISSN:1471-2407
1471-2407
DOI:10.1186/s12885-016-2252-y