Abstract
Cancer stem cells (CSCs) have been implicated in multidrug resistance, a phenomenon responsible for the failure of cancer chemotherapy. However, the underlying mechanisms are still unclear. In our study, we established two oxaliplatin-resistant colorectal cancer cell lines displaying some CSCs characteristics. Oct4 overexpression was observed in these two lines. We performed Oct4 knock down by lentiviral vector-mediated specific shRNA. Knockdown increased apoptosis, decreased CSCs marker expression and weakened tumorigenicity in drug-resistant cell lines. In conclusion, we show that these events can be at least in part attributed to the STAT3/Survivin pathway.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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AC133 Antigen
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Animals
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Antigens, CD / analysis
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Apoptosis*
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Cell Line, Tumor
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Colorectal Neoplasms / drug therapy*
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Colorectal Neoplasms / pathology
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Drug Resistance, Neoplasm
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Glycoproteins / analysis
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Humans
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Hyaluronan Receptors / analysis
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Inhibitor of Apoptosis Proteins / physiology*
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Mice
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Mice, SCID
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Neoplastic Stem Cells / chemistry
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Neoplastic Stem Cells / physiology*
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Octamer Transcription Factor-3 / physiology*
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Organoplatinum Compounds / pharmacology
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Oxaliplatin
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Peptides / analysis
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STAT3 Transcription Factor / physiology*
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Survivin
Substances
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AC133 Antigen
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Antigens, CD
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BIRC5 protein, human
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Glycoproteins
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Hyaluronan Receptors
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Inhibitor of Apoptosis Proteins
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Octamer Transcription Factor-3
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Organoplatinum Compounds
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POU5F1 protein, human
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Peptides
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STAT3 Transcription Factor
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STAT3 protein, human
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Survivin
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Oxaliplatin