Abstract
Dysregulation of apoptosis may be closely related to the development of cancer and its chemoresistance. Overexpression of Bax, an inducer of apoptosis, has led to increased cell death in a variety of cancer cell lines. In this study, we investigated the effect of Bax overexpression in two gastric cancer cell lines, MKN-28 and MKN-45, using a Cre-loxP-mediated inducible expression system. After induction of bax, both cell lines showed decreased proliferation, partially due to increased cell death. Furthermore, Bax-expressing MKN-28 cells were more sensitive to cisplatin. These results indicate that up-regulation of the bax gene may provide a novel strategy for the treatment of gastric cancer.
MeSH terms
-
Adenoviridae / genetics
-
Antineoplastic Agents / pharmacology*
-
Apoptosis / drug effects
-
Apoptosis / genetics
-
Blotting, Northern
-
Cisplatin / pharmacology*
-
Combined Modality Therapy
-
DNA Primers / chemistry
-
Gene Expression / drug effects
-
Gene Expression Regulation
-
Genetic Therapy / methods
-
Humans
-
Integrases / genetics*
-
Proto-Oncogene Proteins / genetics*
-
Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
-
Reverse Transcriptase Polymerase Chain Reaction
-
Stomach Neoplasms / metabolism
-
Stomach Neoplasms / pathology
-
Stomach Neoplasms / therapy*
-
Transcriptional Activation
-
Transfection
-
Tumor Cells, Cultured
-
Viral Proteins*
-
bcl-2-Associated X Protein
Substances
-
Antineoplastic Agents
-
BAX protein, human
-
DNA Primers
-
Proto-Oncogene Proteins
-
Proto-Oncogene Proteins c-bcl-2
-
Viral Proteins
-
bcl-2-Associated X Protein
-
Cre recombinase
-
Integrases
-
Cisplatin