| Project/Area Number |
16591390
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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 |
Thoracic surgery
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
SUZUKI Kazuya Hamamatsu University School of Medicine, First Department of Surgery, Associate Professor, 医学部, 助教授 (00201575)
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| Co-Investigator(Kenkyū-buntansha) |
KITAGAWA Masatoshi Hamamatsu University School of Medicine, First Department of Biochemistry, Professor, 医学部, 教授 (50294971)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | ubiquitin ligase / Pirh2 / p53 / non small-cell lung cancer / anticancer drug sensitivity test / suppressor oncogene |
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| Research Abstract |
Pirh2 was cloned as protein ARNIP which had a RING- finger domain to be connected to an androgen receptor. It is reported that this Pirh2 has ubiquitin ligase activity of p53, and leads p53 to degradation. Cancer growths will be accelerated if resolution of suppressor oncogene products such as p53 is enhanced by ubiquitin ligase activity of Pirh2. However, the roles of Pirh2 in clinical cases were not clear. Therefore we assayed expression of Pirh2 by real time RT-PCR using the non small-cell lung cancer tissues.
Methods :
The cDNA was composed by reverse transcriptase after getting a total RNA from a tissue. Primer was set to exon eight or nine to sandwich intron of a Pirh2 gene. Real time RT-PCR was performed using the primer mentioned above. In addition, degree of expression of Pirh2 and p27 was analysed by immunostaining.
Results :
In 13cases out of 20 adenocarcinoma, Pirh2 was more than double in cancer part tissues comparing with normal lung tissue. Well differentiated adenocarcinoma showed less expression of Pirh2 than moderately-poorly differentiated adenocarcinoma.
In 8cases out of 9 squamous-cell carcinoma, Pirh2 was more than double in cancer tissues comparing with normal lung tissue.
Manifestation of Pirh2 was confirmed in a lung cancer tissue by immunostaining.
Discussion :
High expression of Pirh2 was present in 70% of non small-cell lung cancer.
It is thought that resolution of suppressor oncogene such as p27 and p53 is enhanced by ubiquitination through Pirh2 in non small-cell lung cancer. It was suggested that Pirh2 may contribute to the carcinogenesis or development of lung cancer.
It seems that this research can develop concerning a correlation with clinical characteristics, prognosis, anticancer drug sensitivity test and so on.
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