Abstract
Dysregulation of hedgehog signaling has been involved in esophageal squamous cell carcinoma (ESCC) by the mechanisms that are not fully understood. The receptor for activated protein kinase C (RACK1) is involved in the progression of multiple cancers. However, its expression and function in ESCC have not been investigated. Here, we found that the expression of RACK1 was upregulated in ESCC clinical samples. Moreover, over-expression of RACK1 in ESCC cells promoted cell proliferation and migration, while downregulation of RACK1 impaired the proliferation and migration of ESCC cells in vitro and in vivo. Mechanistically, RACK1 promoted the proliferation and migration of ESCC cells by activating hedgehog signaling. Taken together, our study suggested RACK1 might be an important therapeutic target in ESCC.
MeSH terms
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Animals
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Blotting, Western
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Carcinoma, Squamous Cell / genetics*
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Carcinoma, Squamous Cell / metabolism
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Carcinoma, Squamous Cell / pathology
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Cell Line, Tumor
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Cell Movement / genetics*
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Cell Proliferation
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Disease Progression
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Esophageal Neoplasms / genetics*
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Esophageal Neoplasms / metabolism
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Esophageal Neoplasms / pathology
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GTP-Binding Proteins / genetics*
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GTP-Binding Proteins / metabolism
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Gene Expression Regulation, Neoplastic
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Humans
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Immunohistochemistry
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Luciferases / genetics
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Luciferases / metabolism
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Mice
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Mice, Nude
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Neoplasm Proteins / genetics*
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Neoplasm Proteins / metabolism
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RNA Interference
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Receptors for Activated C Kinase
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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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Xenograft Model Antitumor Assays / methods
Substances
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Neoplasm Proteins
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RACK1 protein, human
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Receptors for Activated C Kinase
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Receptors, Cell Surface
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Luciferases
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GTP-Binding Proteins