2016 Fiscal Year Final Research Report
Mechanism of inhibitory effect of Carbonyl reductase on cancers aiming to gene therapy
Project/Area Number |
26462508
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | Hirosaki University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | Carbonyl reductase / Ovarian cancer / アポトーシス / 腫瘍縮小 / 遺伝子治療 |
Outline of Final Research Achievements |
Tumor growth was significantly suppressed in mice injected with CR1-overexpressing cells. Tumor volume in the CR1 induction group decreased temporarily until 2 weeks. Tumor cell membranes in both CR1 induction and control groups were positive for TNFR1 expression; however, total protein levels did not differ between the two groups. TNFR-2 expression was comparatively weak in both groups. The expression of NF-κB and c-Jun was weaker in the CR1 induction group than in control. In contrast, caspase-8 and caspase-3 expression was higher in the CR1 induction group. Furthermore, the number of apoptotic cells was significantly greater in tumors that appeared after injections of both types of CR1-overexpressing cells than in those of control cancer cells. These results suggest that CR1 induces apoptosis by activating the caspase pathway via binding to TNFR1.
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Free Research Field |
医歯薬学 外科系臨床医学・産婦人科学
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