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Gene Therapy of p53-inactivating tumor by Caspase3

Research Project

Project/Area Number 14571217
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Digestive surgery
Research InstitutionNagoya City University

Principal Investigator

SHINODA Noriyuki  Nagoya City University, Graduate School of Medical Sciences, Research Associate, 大学院・医学研究科, 助手 (80305549)

Co-Investigator(Kenkyū-buntansha) FUJII Yoshitaka  Nagoya City University, Graduate School of Medical Sciences, Professor and Chair, 大学院・医学研究科, 教授 (40156831)
KUWABARA Yoshiyuki  Nagoya City University, Graduate School of Medical Sciences, Assistant Professor, 大学院・医学研究科, 講師 (90225326)
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
KeywordsCaspase3 / apoptosis / XIAP / anti-cancer therapy / VP16 / apotosis / apoptosis / 抗がん剤治療
Research Abstract

Only in the neoplasm cell which p53 was mutated and inactivated, this research devised the system by which Caspase3 is activated, and aimed at improvement in the anti-cancer effect of neoplasm. First, we carried out the cloning of the expression vector of CaspaseS. Moreover, on the cancer cell lines which has p53 mutation, we checked that Caspase3 by this vector was not expressed. Moreover, we checked that included XIAP gene in the down-stream of biding site of p53,expression of XIAP went up on a normal cell line, and expression did not go up on the colon cancer cell stock SW480 with mutant type p53. Next, we checked whether a XIAP vector and a Caspase3 expression vector would be simultaneously introduced into a cancer cell line (wild type p53), and a normal cell line under VP16 existence using these vectors, and apoptosis could be avoided. The analysis of apoptosis was carried out by the increase in subG1 population using FACS. When the XIAP vector and Caspase3 vector were co-transfec … More ted into the human skin normal cell line NHDF, apoptosis was not induced to NHDF. However, when both vectors were transfected into the colon cancer cell line SW480 which has the mutant type p53 under VP16 existence, apoptosis was not induced for four days. Moreover, apoptosis was not induced although transfection was tried to other cell lines, DLD1,HCT116,etc. Although we thought these results that each vector was expressed well, apoptosis has not been induced to cancer-and normal tissues selection system only with these two genes. Although the cause cannot be solved, the relation between that intervention of another factor(s) besides XIAP is mentioned as a candidate and control of XIAP of Caspase3 may have regulation of the delicate amount of expression. In this system, apoptosis was not able to be induced only into the cell which has mutation in p53. If the mechanism of the apoptosis by Caspase3 will become still clearer from now on, we want to carry out cloning to the vector which can fine-adjust change or the amount of expression, or change the vector XIAP to another gene using the same system, and to find the way to the therapy. Less

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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