Abstract
This study aimed to investigate the effect of Helicobacter pylori (H. pylori) infection on the sonic Hedgehog (Shh) signaling in gastric cancer. Shh, Patched (Ptch), and transcription factor Gli1 were overexpressed in H. pylori-infected gastric cancer cells. The oncoprotein, CagA positive H. pylori resulted in significantly higher Shh expression. Pretreatment with MG-132 or PDTC significantly lowered Shh expression. Significant overexpression of Shh and Gli1 were noted in H. pylori-infected compared to non-infected gastric cancer tissues. Conclusively, H. pylori activated the Shh signaling pathway in CagA-dependent manner partly through the NF-kappaB pathway in gastric cancer cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line, Tumor
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Hedgehog Proteins / genetics
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Hedgehog Proteins / metabolism*
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Helicobacter Infections / metabolism*
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Helicobacter Infections / microbiology
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Helicobacter Infections / pathology
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Helicobacter pylori / pathogenicity*
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Humans
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Immunoblotting
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Patched Receptors
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Patched-1 Receptor
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RNA, Messenger / genetics
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / metabolism*
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction
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Stomach Neoplasms / metabolism*
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Stomach Neoplasms / microbiology
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Stomach Neoplasms / pathology
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Transcription Factors / genetics
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Transcription Factors / metabolism*
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Zinc Finger Protein GLI1
Substances
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GLI1 protein, human
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Hedgehog Proteins
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PTCH1 protein, human
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Patched Receptors
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Patched-1 Receptor
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RNA, Messenger
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Receptors, Cell Surface
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SHH protein, human
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Transcription Factors
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Zinc Finger Protein GLI1