| Project/Area Number |
22700921
|
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Clinical oncology
|
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| Research Institution | Kochi University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
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| Keywords | 癌治療 / 糖代謝 / SGLT / 内分泌療法 |
|---|
| Research Abstract |
The epidermal growth factor receptor(EGFR) facilitates glucose transport into cells by associating with and stabilizing a sodium/ glucose cotransporter-1(SGLT-1). In the present study, we have evaluated the effects of Kinase inhibitor : AG1478 and SGLT-1 inhibitor : Phlorizin. We confirmed an expression of SGLT homologs, EGFR, and other key genes for glucose metabolism in ACC cells. In APOPercentage Apoptosis Assay, AG1478 alone induced concentration-dependent tumor cell death, whereas Phlorizin alone has no effect. The combination of AG1478 and Phlorizin exerted the additive inhibitory effect of ACC cell growth. PCR-array Gene Expression Profiling suggested involvement of some gene associated with glucose metabolism such as PPAR associated genes, SNAP25, IFN-γand insulin receptor in this additive inhibitory mechanism. These results demonstrated that the combined use of the EGFR and SGLT-1 antagonists to interfere with glucose metabolism of tumor cells can potentially be effective in the inhibition of ACC cell growth.
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