Yohei Sekino1, Naohide Oue2, Yoshinori Shigematsu1, Akira Ishikawa3, Naoya Sakamoto3, Kazuhiro Sentani3, Jun Teishima4, Akio Matsubara4, Wataru Yasui3. 1. Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan; Department of Urology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan. 2. Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan. Electronic address: naoue@hiroshima-u.ac.jp. 3. Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan. 4. Department of Urology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Abstract
OBJECTIVES: Prostate cancer (PCa) is a common malignancy worldwide. Docetaxel has been an important treatment option for patients with metastatic castration-resistant prostate cancer (CRPC). However, nearly all patients with CRPC treated with docetaxel eventually become refractory. In the present study, we analyzed the expression and distribution of kinesin family member C1 (KIFC1) in human PCa by immunohistochemistry and examined the effect of inhibiting KIFC1 expression on docetaxel resistance. METHODS: Expression of KIFC1 was determined using immunohistochemistry. RNA interference was used to inhibit KIFC1 expression in PCa cell lines. To examine cell viability, we performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. CONCLUSIONS: These results indicate that KIFC1 plays an important role in PCa progression. Immunohistochemical analysis of KIFC1 would facilitate identification of patients with poor prognoses after radical prostatectomy, as well as patients with poor therapeutic outcomes after docetaxel-based chemotherapy.
OBJECTIVES:Prostate cancer (PCa) is a common malignancy worldwide. Docetaxel has been an important treatment option for patients with metastatic castration-resistant prostate cancer (CRPC). However, nearly all patients with CRPC treated with docetaxel eventually become refractory. In the present study, we analyzed the expression and distribution of kinesin family member C1 (KIFC1) in human PCa by immunohistochemistry and examined the effect of inhibiting KIFC1 expression on docetaxel resistance. METHODS: Expression of KIFC1 was determined using immunohistochemistry. RNA interference was used to inhibit KIFC1 expression in PCa cell lines. To examine cell viability, we performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. CONCLUSIONS: These results indicate that KIFC1 plays an important role in PCa progression. Immunohistochemical analysis of KIFC1 would facilitate identification of patients with poor prognoses after radical prostatectomy, as well as patients with poor therapeutic outcomes after docetaxel-based chemotherapy.