A study of the molecule target treatment about survivin, an apoptosis inhibitor, in the prostate and renal cancer.
| Project/Area Number |
20791101
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Gunma University |
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Principal Investigator |
KOIKE Hidekazu Gunma University, 医学部, 助教 (90420091)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 前立腺癌 / 腎癌 / サバイビン |
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| Research Abstract |
We assessed the effect of survivin gene expression on the proliferation of prostate cancer (Pca) cells, and studied the association of suvivin gene expression levels with the pathological grade of Pca. In Pca cells, decrease of survivin gene expression by transfection of siRNA was accompanied by inhibition of cell proliferation of Pca cells. In prostate biopsy samples, survivin expression level of Pca was significantly higher than that of BPH or Pca after androgen deprivation therapy, and was associated significantly with high-grade cancer.
Next, we assessed the effect of survivin gene expression on the proliferation of renal cancer (RCC) cells, and studied the association of suvivin gene expression levels with the clinical stage of RCC. In Caki-1 cells, decrease of Survivin gene expression by transfection of siRNA was accompanied by inhibition of the proliferation. In clinical RCC tissues, survivin expression levels in metastatic stage were significantly higher.
1a,25-dihydroxyvitamin D3 (1,25D) inhibits the proliferation of prostate cancer cells. We examined the antitumor sensitization effect due to survivin inhibition in 1,25D treatment for prostate cancer cells. In LNCaP cells, 1,25D decreased survivin gene expression and inhibited cell proliferation. On the other hand, survivin gene expression and cell proliferation in DU145 cells were not inhibited. However, interestingly, after the transfection of siRNA against survivin, DU145 cell proliferation was inhibited by 1,25D.
These findings suggest that survivin has a significant association with prostate and renal cancer cell proliferation and plays an essential role in 1,25D-induced cell growth inhibition in prostate cancer. It seems that the elimination of survivin in the therapy against prostate and renal cancer is a potential therapeutic option.
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Report
(3 results)
Research Products
(11 results)
