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| 題名: | Protein arginine methyltransferase 5 is a potential oncoprotein that upregulates G1 cyclins/cyclin-dependent kinases and the phosphoinositide 3-kinase/AKT signaling cascade |
| 作者: | 蘇立仁;Wei, Tong‐You W.;Juan, Chi‐Chang;Hisa, Jiun‐Yi;Su, Li‐Jen;Lee, Yuan‐Chii G.;Chou, Hsiang‐Yun;Chen, Jo‐Mei M.;Wu, Yu‐Chung;Chiu, Shao‐Chih;Hsu, Chung‐Ping;Liu, Kuo‐Lin;Yu, Chang‐Tze R. |
| 貢獻者: | 生醫理工學院生醫科學與工程學系 |
| 關鍵詞: | 1-Phosphatidylinositol 3-kinase;AKT protein;Animals;c-Jun amino-terminal kinase;c-Jun protein;Cell adhesion;Cell cycle;Cell density;Cell Line, Tumor;Cell proliferation;Cell Transformation, Neoplastic - genetics;Cell Transformation, Neoplastic - metabolism;cyclin D1;Cyclin-dependent kinase;Cyclin-Dependent Kinases - metabolism;Cyclins;Data processing;G1 Phase;Gene Expression Regulation, Neoplastic;Humans;Lung cancer;Lung Neoplasms - genetics;Lung Neoplasms - metabolism;Mice;Mice, Nude;Oncogene Proteins - genetics;Oncogene Proteins - metabolism;Original;Phosphatidylinositol 3-Kinases - metabolism;phosphoinositides;protein arginine methyltransferase;Protein-Arginine N-Methyltransferases - genetics;Protein-Arginine N-Methyltransferases - metabolism;Proto-Oncogene Proteins c-akt - metabolism;Retinoblastoma protein;Signal Transduction;Statistical analysis;Transcription factors;Tumor cell lines;Tumorigenesis;Western blotting |
| 日期: | 2012-09-01 |
| 上傳時間: | 2026-04-23 11:19:40 (UTC+8) |
| 出版者: | Wiley-Blackwell;England: John Wiley and Sons Inc |
| 摘要: | 摘要： Increasing evidence suggests that PRMT5, a protein arginine methyltransferase, is involved in tumorigenesis. However, no systematic research has demonstrated the cell‐transforming activity of PRMT5. We investigated the involvement of PRMT5 in tumor formation. First, we showed that PRMT5 was associated with many human cancers, through statistical analysis of microarray data in the NCBI GEO database. Overexpression of ectopic PRMT5 per se or its specific shRNA enhanced or reduced cell growth under conditions of normal or low concentrations of serum, low cell density, and poor cell attachment. A stable clone that expressed exogenous PRMT5 formed tumors in nude mice, which demonstrated that PRMT5 is a potential oncoprotein. PRMT5 accelerated cell cycle progression through G1 phase and modulated regulators of G1; for example, it upregulated cyclin‐dependent kinase (CDK) 4, CDK6, and cyclins D1, D2 and E1, and inactivated retinoblastoma protein (Rb). Moreover, PRMT5 activated phosphoinositide 3‐kinase (PI3K)/AKT and suppressed c‐Jun N‐terminal kinase (JNK)/c‐Jun signaling cascades. However, only inhibition of PI3K activity, and not overexpression of JNK, blocked PRMT5‐induced cell proliferation. Further analysis of PRMT5 expression in 64 samples of human lung cancer tissues by microarray and western blot analysis revealed a tight association of PRMT5 with lung cancer. Knockdown of PRMT5 retarded cell growth of lung cancer cell lines A549 and H1299. In conclusion, to the best of our knowledge, we have characterized the cell‐transforming activity of PRMT5 and delineated its underlying mechanisms for the first time.
其他題名： Cancer Sci
出版者： England: John Wiley and Sons Inc
出版日期： 2012-09
出處： Cancer science, 2012-09, Vol.103 (9), p.1640-1650
資源來源： ProQuest
版權： 2012 Japanese Cancer Association
版權： 2012 Japanese Cancer Association.
識別號： ISSN: 1347-9032
識別號： ISSN: 1349-7006
識別號： EISSN: 1349-7006
識別號： DOI: 10.1111/j.1349-7006.2012.02367.x
識別號： PMID: 22726390 |
| 顯示於類別: | [生醫科學與工程學系] 期刊論文
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