| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Sputum samples were collected and preserved. We focused on GRLF1, which is a regulator ofRAS protein and possiblely controlled through microRNAs. By temporal knock-down of GRLF1, significant growth inhibition was observed. However, the effect disappeared when the gene was stably knocked-down. By screening of molecules regarding cell proliferation, both total and phosphorylated protein of STA3 was evidented. In addition, inhibition of STAT3 by a specific tyrosin kinase inhibitor in cells with stable knock-down for GRLF1 induced strong growth inhibition. Thus, we concluded that STAT3 worked as an alternative pathway for cell survival in these cells. These findings indicates that GRLF1 could be a tharapeutic target and STA3 could be a resistant mechanism for that treatment.
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