| Project/Area Number |
26890021
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Tumor therapeutics
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| Research Institution | Osaka City University |
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Principal Investigator |
Tanaka Masako 大阪市立大学, 大学院医学研究科, 特任助教 (00733651)
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 薬剤耐性 / 熱ショックタンパク質 / インタラクトーム / 膵癌 |
|---|
| Outline of Final Research Achievements |
We established cell lines tolerant to serum starvation (PANC-1/Stv) and hypoxia (PANC-1/Hyp) from the parental cell line PANC-1. The IC50 values of gemcitabine for PANC-1/Stv and PANC-1/Hyp cells (under non-stressful conditions) was 142- and 37-fold higher, respectively, than that for the parental cells. These cell lines developed this resistance to gemcitabine via suppression of apoptosis, which is a mechanism of resistance that is common to that of the cell line (PANC-1/GEM) with acquired gemcitabine resistance. However, drug resistance in PANC-1/GEM cells was primarily caused by gemcitabine inactivation. We then compared HSP72 interactome of PANC-1/GEM cells to PANC-1/Stv and PANC-1/Hyp cells, resulting in identification of 37 molecules unique to intrinsic resistance to gemcitabine.
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