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A very low toxic agent induces apoptosis and reduces growth of human hepatocellular carcinoma cells
Author(s) -
Schumacher Guido,
Scheunert Sylvia,
Rueggeberg Anne,
Bachem Max G.,
Nussler Andreas K.,
Spinelli Antonino,
Mukhopadhyay Tapas,
Pratschke Johann,
Neuhaus Peter
Publication year - 2006
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2006.04327.x
Subject(s) - apoptosis , hepatocellular carcinoma , medicine , in vitro , cancer research , cell growth , cell culture , 2 methoxyestradiol , carcinoma , cancer cell , cell , liver cancer , growth inhibition , programmed cell death , cancer , pathology , biology , biochemistry , genetics
Aim: To examine the efficacy on growth inhibition of 2‐methoxyestradiol (2‐ME) on human hepatocellular carcinoma in vitro . Methods: Hep3B, SK‐Hep1, and PLC/PRF/5 cells were used. Proliferation assays using 2‐ME should show a dose‐dependent reduction of cell number. Different staining methods in cells derived from human hepatocellular carcinoma and normal human hepatocytes were performed to demonstrate possible tumor specific induction of apoptosis. FACS‐analysis was done to confirm the induction of apoptosis after treatment with 2‐ME. Results: A reduction of the cell number of 90–98% was observed in all cancer cells after treatment with 2 µmol 2‐ME. The mechanism of action appeared to be induction of apoptosis. Normal human hepatocytes were unaffected by 2‐ME. The most sensitive cell line to 2‐ME, SK‐Hep1, showed an up‐regulation of the p53 and p21 proteins. Conclusions: 2‐Methoxyestradiol appears to be highly effective in reducing tumor growth in vitro in human hepatocellular carcinoma. It may be tumor specific and applicable for clinical trials.