2017 Fiscal Year Final Research Report
Developments of novel treatments based on inhibiting glycolysis with PPARG agonist
| Project/Area Number |
16K19942
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | PPAR / GLUT1 / GLUT1阻害剤 / CDK6 / 抗癌剤感受性 / 細胞周期 / Warburg effect / 癌代謝 |
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| Outline of Final Research Achievements |
Peroxisome proliferator-activated receptor-gamma (PPARγ) is a tumor suppresser gene. Glucose transporter type 1 (Glut1) plays a crucial role in cancer specific metabolism to adapt to the rapid growth and tumor microenvironment. The proliferation of the esophageal squamous cell carcinoma (ESCC) cell lines were inhibited (20-70%) using small interfering (si) iRNA for GLUT1. CDK6 mRNA level significantly reduced and p27 kip mRNA level significantly increased after si-RNA for GLUT1. The anti-proliferative effect of low dose cisplatin was not detected in TE11 after control si-RNA, however low dose cisplatin exerted anti-proliferative effect after si-RNA for GLUT1. PKM2 and LDHA mRNA levels which are associated with glycolysis significantly decreased and PPARγ mRNA levels increased. The new GLUT1 inhibitor exerted a strong antitumor effect with low concentration and an additive effect with combined with cisplatin.
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| Free Research Field |
消化器外科
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