Abstract
The putative tumor suppressor Mst1, when cleaved to its 36kDa cleaved form, amplifies apoptotic signals. We found that Mst1 was predominantly expressed in its full-length form in 76% (17/25 cases) of hepatocellular carcinoma (HCC) tumors. Mst1 cleavage was basically absent in HCC cells. Ectopic full-length Mst1 expression increased the growth of HCC cells by 55-80% within 3days after transfection. Expression of exogenous NORE1B, a tumor suppressor commonly lost in HCC tumors (~56% of our cohort), was sufficient to suppress the growth promotion of full-length Mst1. Hence, Mst1 exhibits a growth promoting activity in HCC cells upon NORE1B downregulation.
Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptor Proteins, Signal Transducing
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Apoptosis
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Apoptosis Regulatory Proteins
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Carcinoma, Hepatocellular / metabolism*
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Carcinoma, Hepatocellular / pathology
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Cell Line, Tumor
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Cell Proliferation*
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Cell Survival
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DNA Mutational Analysis
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Gene Expression
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Gene Expression Regulation, Neoplastic
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HEK293 Cells
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Hepatocyte Growth Factor / genetics
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Hepatocyte Growth Factor / metabolism
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Hepatocyte Growth Factor / physiology*
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Humans
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Liver Neoplasms / metabolism*
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Liver Neoplasms / pathology
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Molecular Weight
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Monomeric GTP-Binding Proteins / genetics
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Monomeric GTP-Binding Proteins / metabolism
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Proteolysis
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins / physiology*
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Up-Regulation
Substances
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Adaptor Proteins, Signal Transducing
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Apoptosis Regulatory Proteins
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Proto-Oncogene Proteins
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RASSF5 protein, human
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macrophage stimulating protein
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Hepatocyte Growth Factor
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Monomeric GTP-Binding Proteins