| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Profilaggrin plays a critical role in keratinocyte terminal differentiation. During this process, a 55-kDa N-terminal fragment of profilaggrin (FLG-N) is translocated into the nucleus; thereafter, the cells became TUNEL-positive. We examined the molecular mechanism underlying the DNA degradation process induced by FLG-N in keratinocytes. Our findings suggest that calpine I and apoptosis-inducing factor may be associated with the FLG-N inducing-DNA degradation. We also found that FLG-N directly interacted with pinin, a transcriptional activator binding to the E-box 1 core sequence of the E-cadherin promoter gene, within the nucleus. Surprisingly, the suppression of pinin expression can induce cell death in keratinocytes even without interaction with FLG-N. In addition, 19 amino acids present in the N-terminal profilaggrin can induce cell death for squamous cell carcinoma (SCC) cell line HSC-1. We therefore hypothesized that FLG-N may be a novel therapeutic target in SCC.
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