| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Research Abstract |
Despite recent advances in various chemotherapeutic regimens, pancreatic cancer remains highly resistant to conventional chemotherapy. The putative tunor suppressor RBM5 is known to modulate apoptosis and cell cycle arrest but the molecular mechanisms of RBM5 function are poorly understood.
We show here that RBM5 interacted with HuR, which is one of mRNA regulatory proteins that bind AU-rich elements in the 3'-untranslated regions of target mRNAs, stabilizing them and modulating their translation. Certain cell stresses including chemotherapeutic reagents induce translocation of HuR from the nucleus to the cytoplasm. RBM5 associated with HuR in the nucleus and reduced translocation of HuR to the cytoplasm. Furthermore, RBM5 overexpression decreased the association of HuR with target mRNAs.
Taken together, we suggest that RBM5 might play important roles in the post-transcriptional regulation of mRNAs that are involved in the metabolism of chemotherapeutic reagents.
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