Abstract
Inhibition of Wnt/beta-catenin pathway is an attractive method for therapy of various tumors including breast, colorectal, and cervical cancer, etc. However, little is known about the role of Wnt2/beta-catenin pathway in esophageal squamous cell carcinoma (ESCC). Here we identify that Wnt2/beta-catenin signaling pathway is activated in ESCC cells, and sodium nitroprusside (SNP) and siRNA against beta-catenin not only inhibit the expressions of beta-catenin and its major downstream effectors including c-myc and cyclin D1, but induce cell cycle arrest and apoptosis, suggesting that Wnt2/beta-catenin pathway may be a potential molecular target for ESCC therapy.
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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Carcinoma, Squamous Cell / drug therapy
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Carcinoma, Squamous Cell / metabolism*
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Carcinoma, Squamous Cell / pathology
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Cell Cycle / drug effects
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Cell Line, Tumor
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Esophageal Neoplasms / drug therapy
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Esophageal Neoplasms / metabolism*
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Esophageal Neoplasms / pathology
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Humans
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Nitroprusside / pharmacology*
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RNA, Messenger / analysis
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RNA, Small Interfering / pharmacology
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Signal Transduction / physiology*
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Wnt2 Protein / antagonists & inhibitors
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Wnt2 Protein / genetics
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Wnt2 Protein / metabolism*
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beta Catenin / antagonists & inhibitors
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beta Catenin / genetics
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beta Catenin / metabolism*
Substances
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RNA, Messenger
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RNA, Small Interfering
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WNT2 protein, human
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Wnt2 Protein
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beta Catenin
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Nitroprusside