Abstract
Drug resistance is the leading cause of chemotherapy failure in the treatment of ovarian cancer. So far, little is known about the mechanism of chemoresistance in ovarian cancer. In this study, we explored the mechanism that HSP27 was involved in cisplatin resistance of ovarian cancer both in vitro and clinically. HSP27 protein was found to be upregulated and expressed in cisplatin-resistant ovarian cancer cell line C13*, and HSP27 siRNA transfection reversed the chemoresistance of C13*. We found that HSP27 exerted its chemoresistant role by inhibiting p21 transferring from the nucleus to the plasma through the activation of phosphorylated-Akt pathway. These findings have implications for clinical trials aimed at a potential therapeutic target for ovarian tumors that are refractory to conventional treatment.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / drug effects
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Cell Nucleus / genetics
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Cell Nucleus / metabolism
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Cisplatin / administration & dosage
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Cytoplasm / genetics
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Cytoplasm / metabolism
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Drug Resistance, Neoplasm / genetics*
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Female
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Gene Knockdown Techniques
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HSP27 Heat-Shock Proteins / antagonists & inhibitors
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HSP27 Heat-Shock Proteins / biosynthesis
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HSP27 Heat-Shock Proteins / genetics*
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Heat-Shock Proteins
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Humans
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Molecular Chaperones
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Ovarian Neoplasms / drug therapy*
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Ovarian Neoplasms / genetics
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Ovarian Neoplasms / pathology
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Proto-Oncogene Proteins c-akt / genetics
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RNA, Small Interfering / genetics
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p21-Activated Kinases / biosynthesis*
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p21-Activated Kinases / genetics
Substances
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HSP27 Heat-Shock Proteins
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HSPB1 protein, human
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Heat-Shock Proteins
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Molecular Chaperones
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RNA, Small Interfering
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Proto-Oncogene Proteins c-akt
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p21-Activated Kinases
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Cisplatin