FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway

C. H. Chen, P. J. Lu, Y. C. Chen, S. L. Fu, K. J. Wu, A. P. Tsou, Y. C G Lee, T. C E Lin, S. L. Hsu, W. J. Lin, C. Y F Huang, C. K. Chou

研究成果: 雜誌貢獻文章

55 引文 (Scopus)

摘要

A significant challenge in the post-genomic era is how to prioritize differentially expressed and uncharacterized novel genes found in hepatocellular carcinoma (HCC) microarray profiling. One such category is cell cycle regulated genes that have only evolved in higher organisms but not in lower eukaryotic cells. Characterization of these genes may reveal some novel human cancer-specific abnormalities. A novel transcript, FLJ10540 was identified. FLJ10540 is overexpressed in HCC as examined by quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. The patients with higher FLJ10540 expression had a poor survival than those with lower FLJ10540 expression. Functional characterization indicates that FLJ10540 displays a number of characteristics associated with an oncogene, including anchorage-independent growth, enhanced cell growth at low serum levels and induction of tumorigenesis in nude mice. FLJ10540-elicited cell transformation is mediated by activation of the phosphatidylinositol 3′-kinase (PI3K)/AKT pathway. Moreover, FLJ10540 forms a complex with PI3K and can activate PI3K activity, which provides a mechanistic basis for FLJ10540-mediated oncogenesis. Together, using a combination of bioinformatics searches and empirical data, we have identified a novel oncogene, FLJ10540, which is conserved only in higher organisms. The finding raises the possibility that FLJ10540 is a potential new therapeutic target for HCC treatment. These findings may contribute to the development of new therapeutic strategies that are able to block the PI3K/AKT pathway in cancer cells.
原文英語
頁(從 - 到)4272-4283
頁數12
期刊Oncogene
26
發行號29
DOIs
出版狀態已發佈 - 六月 21 2007

指紋

Phosphatidylinositol 3-Kinase
Phosphatidylinositol 3-Kinases
Hepatocellular Carcinoma
Oncogenes
Carcinogenesis
cdc Genes
Eukaryotic Cells
Growth
Computational Biology
Nude Mice
Genes
Reverse Transcription
Neoplasms
Therapeutics
Immunohistochemistry
Polymerase Chain Reaction
Survival
Serum

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

引用此文

Chen, C. H., Lu, P. J., Chen, Y. C., Fu, S. L., Wu, K. J., Tsou, A. P., ... Chou, C. K. (2007). FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway. Oncogene, 26(29), 4272-4283. https://doi.org/10.1038/sj.onc.1210207

FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway. / Chen, C. H.; Lu, P. J.; Chen, Y. C.; Fu, S. L.; Wu, K. J.; Tsou, A. P.; Lee, Y. C G; Lin, T. C E; Hsu, S. L.; Lin, W. J.; Huang, C. Y F; Chou, C. K.

於: Oncogene, 卷 26, 編號 29, 21.06.2007, p. 4272-4283.

研究成果: 雜誌貢獻文章

Chen, CH, Lu, PJ, Chen, YC, Fu, SL, Wu, KJ, Tsou, AP, Lee, YCG, Lin, TCE, Hsu, SL, Lin, WJ, Huang, CYF & Chou, CK 2007, 'FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway', Oncogene, 卷 26, 編號 29, 頁 4272-4283. https://doi.org/10.1038/sj.onc.1210207
Chen, C. H. ; Lu, P. J. ; Chen, Y. C. ; Fu, S. L. ; Wu, K. J. ; Tsou, A. P. ; Lee, Y. C G ; Lin, T. C E ; Hsu, S. L. ; Lin, W. J. ; Huang, C. Y F ; Chou, C. K. / FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway. 於: Oncogene. 2007 ; 卷 26, 編號 29. 頁 4272-4283.
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abstract = "A significant challenge in the post-genomic era is how to prioritize differentially expressed and uncharacterized novel genes found in hepatocellular carcinoma (HCC) microarray profiling. One such category is cell cycle regulated genes that have only evolved in higher organisms but not in lower eukaryotic cells. Characterization of these genes may reveal some novel human cancer-specific abnormalities. A novel transcript, FLJ10540 was identified. FLJ10540 is overexpressed in HCC as examined by quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. The patients with higher FLJ10540 expression had a poor survival than those with lower FLJ10540 expression. Functional characterization indicates that FLJ10540 displays a number of characteristics associated with an oncogene, including anchorage-independent growth, enhanced cell growth at low serum levels and induction of tumorigenesis in nude mice. FLJ10540-elicited cell transformation is mediated by activation of the phosphatidylinositol 3′-kinase (PI3K)/AKT pathway. Moreover, FLJ10540 forms a complex with PI3K and can activate PI3K activity, which provides a mechanistic basis for FLJ10540-mediated oncogenesis. Together, using a combination of bioinformatics searches and empirical data, we have identified a novel oncogene, FLJ10540, which is conserved only in higher organisms. The finding raises the possibility that FLJ10540 is a potential new therapeutic target for HCC treatment. These findings may contribute to the development of new therapeutic strategies that are able to block the PI3K/AKT pathway in cancer cells.",
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AU - Lu, P. J.

AU - Chen, Y. C.

AU - Fu, S. L.

AU - Wu, K. J.

AU - Tsou, A. P.

AU - Lee, Y. C G

AU - Lin, T. C E

AU - Hsu, S. L.

AU - Lin, W. J.

AU - Huang, C. Y F

AU - Chou, C. K.

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N2 - A significant challenge in the post-genomic era is how to prioritize differentially expressed and uncharacterized novel genes found in hepatocellular carcinoma (HCC) microarray profiling. One such category is cell cycle regulated genes that have only evolved in higher organisms but not in lower eukaryotic cells. Characterization of these genes may reveal some novel human cancer-specific abnormalities. A novel transcript, FLJ10540 was identified. FLJ10540 is overexpressed in HCC as examined by quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. The patients with higher FLJ10540 expression had a poor survival than those with lower FLJ10540 expression. Functional characterization indicates that FLJ10540 displays a number of characteristics associated with an oncogene, including anchorage-independent growth, enhanced cell growth at low serum levels and induction of tumorigenesis in nude mice. FLJ10540-elicited cell transformation is mediated by activation of the phosphatidylinositol 3′-kinase (PI3K)/AKT pathway. Moreover, FLJ10540 forms a complex with PI3K and can activate PI3K activity, which provides a mechanistic basis for FLJ10540-mediated oncogenesis. Together, using a combination of bioinformatics searches and empirical data, we have identified a novel oncogene, FLJ10540, which is conserved only in higher organisms. The finding raises the possibility that FLJ10540 is a potential new therapeutic target for HCC treatment. These findings may contribute to the development of new therapeutic strategies that are able to block the PI3K/AKT pathway in cancer cells.

AB - A significant challenge in the post-genomic era is how to prioritize differentially expressed and uncharacterized novel genes found in hepatocellular carcinoma (HCC) microarray profiling. One such category is cell cycle regulated genes that have only evolved in higher organisms but not in lower eukaryotic cells. Characterization of these genes may reveal some novel human cancer-specific abnormalities. A novel transcript, FLJ10540 was identified. FLJ10540 is overexpressed in HCC as examined by quantitative reverse transcription-polymerase chain reaction and immunohistochemistry. The patients with higher FLJ10540 expression had a poor survival than those with lower FLJ10540 expression. Functional characterization indicates that FLJ10540 displays a number of characteristics associated with an oncogene, including anchorage-independent growth, enhanced cell growth at low serum levels and induction of tumorigenesis in nude mice. FLJ10540-elicited cell transformation is mediated by activation of the phosphatidylinositol 3′-kinase (PI3K)/AKT pathway. Moreover, FLJ10540 forms a complex with PI3K and can activate PI3K activity, which provides a mechanistic basis for FLJ10540-mediated oncogenesis. Together, using a combination of bioinformatics searches and empirical data, we have identified a novel oncogene, FLJ10540, which is conserved only in higher organisms. The finding raises the possibility that FLJ10540 is a potential new therapeutic target for HCC treatment. These findings may contribute to the development of new therapeutic strategies that are able to block the PI3K/AKT pathway in cancer cells.

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