Abstract
Purpose:
The purpose of this study was to determine the impact of sorafenib on PI3K/AKT/mTOR signaling pathway and to further define its mechanism for treating hepatocellular carcinoma (HCC).
Methods:
Human SMMC-7721 hepatic carcinoma cells were treated with or without 4 μmoL/L sorafenib. SMMC- 7721 cells were harvested at various time points (0-48 hrs) and assessed for changes in PI3K, mTOR, and AKT protein and mRNA levels.
Results:
Human SMMC-7721 hepatic tumor cells exposed to sorafenib had decreased expression of PI3K/mTOR/AKT.
Conclusion:
Sorafenib appears to inhibit hepatic tumor growth by downregulating PI3k/Akt/mTOR signaling pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / pharmacology*
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Cell Line, Tumor
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Down-Regulation
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Humans
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Liver Neoplasms / enzymology*
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Liver Neoplasms / genetics
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Liver Neoplasms / pathology
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Niacinamide / analogs & derivatives*
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Niacinamide / pharmacology
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Phenylurea Compounds / pharmacology*
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Phosphatidylinositol 3-Kinase / genetics
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Phosphatidylinositol 3-Kinase / metabolism
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Phosphoinositide-3 Kinase Inhibitors*
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Protein Kinase Inhibitors / pharmacology*
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Proto-Oncogene Proteins c-akt / agonists*
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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RNA, Messenger / metabolism
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Signal Transduction / drug effects*
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Sorafenib
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TOR Serine-Threonine Kinases / antagonists & inhibitors*
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TOR Serine-Threonine Kinases / genetics
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TOR Serine-Threonine Kinases / metabolism
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Time Factors
Substances
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Antineoplastic Agents
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Phenylurea Compounds
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Phosphoinositide-3 Kinase Inhibitors
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Protein Kinase Inhibitors
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RNA, Messenger
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Niacinamide
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Sorafenib
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MTOR protein, human
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Phosphatidylinositol 3-Kinase
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Proto-Oncogene Proteins c-akt
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TOR Serine-Threonine Kinases