2004 Fiscal Year Final Research Report Summary
The analysis of a novel gene E6DG1 function involving in anchorage dependency
| Project/Area Number |
14570116
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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 |
Pathological medical chemistry
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| Research Institution | Chiba University |
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Principal Investigator |
SHIRASAWA Hiroshi Chiba Univ., Graduate School of Medicine, professor, 大学院・医学研究院, 教授 (00216194)
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| Co-Investigator(Kenkyū-buntansha) |
KOSEKI Akihiko Chiba Univ., Graduate School of Medicine, professor, 大学院・医学研究院, 教授 (40225446)
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| Project Period (FY) |
2002 – 2004
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| Keywords | anchorage dependence / HPV / E6 / Rlp7p / ribosome related protein |
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| Research Abstract |
We identified a novel gene, the expression of which is downregulated by the human papillomavirus 16(HPVI6) E6 protein, and designated E6DG1. In this study, we aimed at the analysis of the E6DG1 functions.
The overexpression of the E6DG1 suppressed the anchorage dependency of cancer cells. In contrast, the downregulation of E6DG1 caused the enhancement of the anchorage dependency of several cancer cells, and had no effect on the anchorage dependency of HeLa cells. It was supposed that the pathway involved in E6DG1 may be disturbed in HeLa cells. Both the overexpression and downregulation of E6DG1 also induced apoptosis.
The analysis of E6DG1 revealed that this protein is ribosomal protein related and has homology to 60S L7. The E6DG1 has a domain which is similar to that found in yeast Rlp7p, a ribosomal protein related protein. Our analysis indicated that the E6DG1 has a critical function involved in the biogenesis of ribosome as the yeast Rlp7p.
It was suggested that the E6DG1 is a ribosome-related protein involving in the processing of the ribosome biogenesis, affecting the anchorage dependency. We propose that the E6DG1 might also affect the chromosomal instability through interacting with the cell cycle and apoptosis. This supposed mechanism of the chromosomal instability induced by disturbing the ribosomal biogenesis would provide an insight into a novel mechanism of oncogenesis.
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