Abstract
Through analysis of the detailed genome-wide gene expression profiles of 81 breast tumors, we identified a novel gene, G-patch domain containing 2 (GPATCH2), that was overexpressed in the great majority of breast cancer cases. Treatment of breast cancer cells MCF-7 and T47D with siRNA against GPATCH2 effectively suppressed its expression, and resulted in the growth suppression of cancer cells, suggesting its essential role in breast cancer cell growth. We found an interaction of GPATCH2 protein with hPrp43, an RNA-dependent ATPase. Their interaction could significantly enhance the ATPase activity of hPrp43 and induce a growth-promoting effect on mammalian cells. Because northern blot analyses of normal human organs implied GPATCH2 to be a novel cancer/testis antigen, targeting GPATCH2 or inhibition of the interaction between GPATCH2 and hPrp43 could be a promising novel therapeutic strategy of breast cancer.
MeSH terms
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Adenosine Triphosphatases / genetics
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Adenosine Triphosphatases / metabolism*
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Antigens, Neoplasm / genetics
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Antigens, Neoplasm / immunology
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Antigens, Neoplasm / metabolism*
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Breast Neoplasms / genetics
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Breast Neoplasms / metabolism*
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Breast Neoplasms / pathology
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Carrier Proteins / genetics
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Carrier Proteins / immunology
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Carrier Proteins / metabolism*
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Cell Line
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Cell Line, Tumor
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Cell Proliferation
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Escherichia coli / genetics
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Female
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Gene Expression Profiling
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Gene Expression Regulation, Neoplastic
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Gene Silencing
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Humans
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Immunohistochemistry
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Immunoprecipitation
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Kidney / cytology
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Male
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Mass Spectrometry
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Neoplasm Proteins / genetics
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Neoplasm Proteins / immunology
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Neoplasm Proteins / metabolism*
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RNA Helicases / genetics
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RNA Helicases / metabolism*
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RNA, Small Interfering / pharmacology
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Recombinant Proteins / metabolism
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Testis / metabolism
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Transfection
Substances
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Antigens, Neoplasm
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Carrier Proteins
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GPATCH2 protein, human
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Neoplasm Proteins
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RNA, Small Interfering
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Recombinant Proteins
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DHX15 protein, human
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Adenosine Triphosphatases
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RNA-dependent ATPase
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RNA Helicases