Effect of microenvironment on progression of CRPC and on docetaxel-resistance

• Project/Area Number: 25462473
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Kanazawa University
• Principal Investigator: KADONO Yoshifumi 金沢大学, 大学病院, 助教 (10397218)
• Co-Investigator(Kenkyū-buntansha): MIZOKAMI Atsushi 金沢大学, 医学系, 准教授 (50248580) ; KITAGAWA Yasuhide 金沢大学, 大学病院, 講師 (00452102)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000); Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000); Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
• Keywords: 前立腺癌 / カバジタキセル耐性株 / 間質細胞 / 微小環境 / パクリタキセル耐性

Outline of Final Research Achievements

Although chemotherapy using docetaxel is conducted for castration-resistant prostate cancer (CRPC) after androgen-deprivation therapy, CRPC become resistant for docetaxel again. We hypothesized that the mechanism is related with tumor microenvironment. Then we co-cultured androgen-independent prostate cancer PC-3 with cancer-associated fibroblast (CAF) and investigated whether CAF affect docetaxel-sensitivity. However, CAF did not affect DOC-sensitivity.
Next, we hypothesized that CAF derived from CRPC is different from CAF from androgen-naive prostate cancer. Then we made gene expression profiles from CAF derived from CRPC and CAF from androgen-naive prostate cancer. We identified several differentially expressed genes. Now we are confirming whether these genes are related with CRPC progression.