Identifying miRNAs associate for Gemcitabine resistance of bladder cancer and elucidating functional roles of their target genes.

• Project/Area Number: 25861416
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Urology
• Research Institution: Gifu University
• Principal Investigator: KATO Taku 岐阜大学, 医学(系)研究科(研究院), 助教 (50596202)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000); Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
• Keywords: 膀胱癌 / 塩酸ゲムシタビン / Androgen receptor / miRNA / Androgen Receptor / エンザルタミド / mi-RNA

Outline of Final Research Achievements

We generated gemcitabine-resistant T24GR bladder cancer cells from parental T24 cells. mRNA microarray analyses showed Androgen receptor (AR) expression was higher among T24GR cells than parental T24 cells. Western blotting analysis also showed AR protein expression level was higher in T24GR. To asses the influences of androgen to AR positive T24GR cells, we cultured cells under androgen depletion or enzalutamide, one of the anti-androgen drug. Androgen depletion and enzalutamide attenuated bladder cancer cell proliferation among T24GR cells compared to parental T24 cells.
We hypothesized AR could be a novel therapeutic target to gemcitabine-resistant bladder cancer. Now we are studying functional role of AR among gemcitabine-resistant bladder cancer and miRNAs targeting AR.