2013 Fiscal Year Final Research Report
Study on the possible roles of calcium sensor, stromal interaction molecule 1 (STIM1), in human epidermoid carcinoma cell growth
| Project/Area Number |
23590311
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
YOSHIDA Junko 金沢医科大学, 医学部, 講師 (20064628)
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| Co-Investigator(Renkei-kenkyūsha) |
IWABUCHI Kuniyoshi 金沢医科大学, 医学部, 教授 (10232696)
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| Project Period (FY) |
2011 – 2013
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| Keywords | ストア作動性カルシウム流入 / STIM1 / cell proliferation / cell migration / tumorigenicity / ヒト扁平上皮がん |
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| Research Abstract |
Stromal interaction molecule 1 (STIM1) monitors the calcium levels in the endoplasmic reticulum and activates the plasma membrane calcium release-activated calcium (CRAC) channels to induce the store operated calcium entry (SOCE). To explore the posible roles of STIM1 in human epidermoid carcinoma A431 cell growth, we established the STIM1 knockdown A431 clones by RNA interference. The SOCE, cell proliferation, cell migration and the xenograft growth in nude mice were reduced in the knockdown clones compared to a negative control clone. Re-expression of a siRNA-resistant full-length STIM1, but not CRAC activation domain (CAD)-deleted STIM1 mutant, in the knockdown clones restored the amplitude of SOCE and cell migration. These results indicate that STIM1 plays an important role in SOCE, cell growth and tumorigenicity in human epidermoid A431 cells, suggesting the potential use of STIM1-targeting agents for treating epidermoid carcinoma.
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