| Project/Area Number |
16K21203
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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 |
General pharmacology
Medical pharmacy
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Research Collaborator |
MASAKI Tsutomu
IWAMA Hisakazu
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | テルミサルタン / 食道癌 / マイクロRNA / 細胞周期 / アポトーシス / バレット食道癌 / アンジオテンシン受容体拮抗薬 / 食道腺癌 / バレット腺癌 / アンギオテンシンII受容体拮抗薬 / バレット食道腺癌 / 降圧薬 / マイクロアレイ / シグナル伝達 |
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| Outline of Final Research Achievements |
Telmisartan, a widely used antihypertensive drug, is an angiotensin II type 1 (AT1) receptor blocker (ARB). This drug inhibits cancer cell proliferation, but the underlying mechanisms in various cancers, remain unknown. The aim of the present study was to evaluate the effects of telmisartan on human esophageal cancer cell proliferation in vitro and in vivo.
We assessed the effects of telmisartan on human esophageal adenocarcinoma cells. Telmisartan inhibited the proliferation of these three cell lines via blockade of the G0 to G1 cell cycle transition. This blockade was accompanied by a strong decrease in cyclin E, and other cell cycle-related proteins. Notably, the AMP-activated protein kinase (AMPK) pathway was enhanced by telmisartan. Furthermore, miRNA expression was significantly altered by telmisartan in vitro and in vivo. In conclusion, telmisartan suppressed human EAC cell proliferation and tumor growth by inducing cell cycle arrest via the AMPK/mTOR pathway.
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