| Project/Area Number |
13671361
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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 |
Digestive surgery
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| Research Institution | Kurume University |
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Principal Investigator |
FUJII Teruhiko KURUME UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (50199288)
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| Co-Investigator(Kenkyū-buntansha) |
YAMANA Hideaki KURUME UNIVERSITY, SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (30140669)
SUEYOSHI Susumu KURUME UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (30235840)
主藤 朝也 久留米大学, 医学部, 助手 (50309803)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | esophageal cancer / protein kinase C / b2 chimaerin / protein kinase C(PKC) / β2chimaerin |
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| Research Abstract |
PKC and β2chimaerin play important role in intracellular signaling, however, the role of PKC and β2chimaerin are not clear in esophageal cancer cells. The aim of this study was to explore the role of PKCδ and β2chimaerin as a mediator of phorbor ester-mediated responses in KE3 esophageal cancer cells. The phorbor ester PMA induces G_2 cell cycle arrest in KE3 esophageal cancer cells. A significant inhibition in cell number was observed upon infection with PKCδAdV, however, β2chimaerin overexpression did not cause any significant changes in cell number or cell cycle ditribution. PKCδ is closely involved in PMA-induced inhibition in KE3 cell growth. The results. of the experiments with ChimAdV exclude the possibility of β2chimaerin involvement. However, β2chimaerin plays important role in intracellular signaling, further study is required.
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