Abstract
Excision repair cross complementation group-1 (ERCC1) was reported to be responsible for drug resistance during cancer treatment. In this report, we first proved the existence of ERCC1 exon VIII alternative splicing in ovarian cancer cells. Further investigation showed that over-expressed exon VIII deficient ERCC1 variant failed to change the protein level of ERCC1 in cancer cells, but decreased the excision repair function of ERCC1 and enhanced sensitivity of cancer cells to cisplatin in a dose-dependent manner. The results indicate that ERCC1 exon VIII alternative splicing does exist in some ovarian cancer cell lines, and regulates cisplatin-resistance in ovarian cancer cells.
MeSH terms
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Alternative Splicing*
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Antineoplastic Agents / pharmacology*
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Cell Survival / drug effects
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Cisplatin / pharmacology*
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DNA Damage
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / metabolism
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Dose-Response Relationship, Drug
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Drug Resistance, Neoplasm / genetics*
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Endonucleases / genetics*
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Endonucleases / metabolism
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Exons
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Female
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Gene Expression Regulation, Enzymologic*
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Gene Expression Regulation, Neoplastic*
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Humans
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Ovarian Neoplasms / enzymology
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Ovarian Neoplasms / genetics*
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Ovarian Neoplasms / pathology
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Reproducibility of Results
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Transfection
Substances
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Antineoplastic Agents
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DNA-Binding Proteins
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ERCC1 protein, human
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Endonucleases
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Cisplatin