Abstract
The transforming growth factor β (TGF-β) pathway acts as a double-edged sword in tumorigenesis. By constraining epithelial cell growth, TGF-β is a potent tumor suppressor. However, TGF-β also acts as a key player in the induction of epithelial-to-mesenchymal transition (EMT), thereby enhancing invasiveness and metastasis. Furthermore, TGF-β signaling has recently been correlated with resistance against both targeted and conventional anticancer agents. Here, we present data demonstrating a role for TGF-β in chemotherapy resistance in colorectal cancer (CRC). We discuss these results in the context of recent findings indicating TGF-β signaling as an emerging player in cancer drug resistance.
Keywords:
EMT; TGF-β; chemotherapy; drug resistance.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / therapeutic use
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Antineoplastic Agents / toxicity
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Apoptosis / drug effects
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Cell Line, Tumor
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Colorectal Neoplasms / drug therapy
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Colorectal Neoplasms / metabolism
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Colorectal Neoplasms / pathology
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Drug Resistance, Neoplasm*
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Epithelial-Mesenchymal Transition
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Humans
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Mediator Complex / antagonists & inhibitors
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Mediator Complex / genetics
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Mediator Complex / metabolism
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RNA Interference
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RNA, Small Interfering / metabolism
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Signal Transduction / drug effects
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Smad2 Protein / metabolism
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Smad3 Protein / metabolism
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Transforming Growth Factor beta / antagonists & inhibitors
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Transforming Growth Factor beta / metabolism*
Substances
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Antineoplastic Agents
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MED12 protein, human
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Mediator Complex
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RNA, Small Interfering
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Smad2 Protein
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Smad3 Protein
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Transforming Growth Factor beta