2005 Fiscal Year Final Research Report Summary
Human DEAD-box/RNA helicase rck/p54 contributes to maintenance of cell growth by affecting cell cycle in cultured cells
| Project/Area Number |
16590334
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Gifu International Institute of Biotechnology |
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Principal Investigator |
AKAO Yukihiro Gifu International Institute of Biotechnology, Medical Oncology, Manager, 部長 (00222505)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAGAWA Yoshihiko Gifu International Institute of Biotechnology, Medical Oncology, Researcher, 研究員 (60372108)
MATSUMOTO Kenji Gifu International Institute of Biotechnology, Natural product, Researcher, 研究員 (60288701)
USUKURA Jiro Nagoya University of Medicine, Anatomy, Associate Professor, 大学院・医学研究科, 助教授 (30143415)
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| Project Period (FY) |
2004 – 2005
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| Keywords | translation initiation / degradation of mRNAs / rck / p54 / cell proliferation / DAED-box RNA helicase / cell cycle / carcinogenesis / genes associated with chromosome translocation |
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| Research Abstract |
Understanding the control of gene expression in cancer cells requires defining the molecular and cellular basis of RNA metabolism compared with that in steady-state normal cells. Previously, we reported evidence that human RNA structure-modifying unwindase rck/p54, a member of DEAD-box family, was highly expressed in most of the malignant cell lines tested and that this expression was linked to malignant transformation. Here, we show that rck/p54 positively affects cell growth, probably by modulating the gene expression at the translational level in cultured cells. In cell growth and differentiation induced by external stimuli, the level of rck/p54 expression was up-regulated during cell proliferation and down-regulated during differentiation. The down-regulation of rck/p54 in HeLa cells by RNAi inhibited cell growth through cell cycle arrest at S phase. Immunoprecipitation using anti-rck/p54 antibody and HeLa cells demonstrated the co-precipitation of rck/p54 with eIF4E, which is well known to bind to the 5'cap-structure, resulting in initiation of translation. These data suggest that rck/p54 contributes to cell growth possibly by modulating translation-initiation control of the genes involved in the cell proliferation, which is a newly defined mechanism leading to carcinogenesis.
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