KIFC1 induces resistance to docetaxel and is associated with survival of patients with prostate cancer.
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.



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.



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.
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.
Yohei
Y
Sekino
Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan. Electronic address: naoue@hiroshima-u.ac.jp.
Naohide
N
Oue
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.
Yoshinori
Y
Shigematsu
Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Akira
A
Ishikawa
Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Naoya
N
Sakamoto
Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Kazuhiro
K
Sentani
Department of Urology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Jun
J
Teishima
Department of Urology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Akio
A
Matsubara
Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
Wataru
W
Yasui
D000368:Aged; D000970:Antineoplastic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001808:Blood Vessels / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D018572:Disease-Free Survival; D000077143:Docetaxel; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D055785:Gene Knockdown Techniques; D006801:Humans; D018960:Hyaluronan Receptors / Q000378:metabolism; D016547:Kinesins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D060787:Neoplasm Grading; D009361:Neoplasm Invasiveness; D014411:Neoplastic Stem Cells / Q000378:metabolism; D011467:Prostate / Q000378:metabolism; D064129:Prostatic Neoplasms, Castration-Resistant / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering; D012189:Retrospective Studies; D018874:Spheroids, Cellular / Q000187:drug effects; D043823:Taxoids / Q000494:pharmacology* / Q000627:therapeutic use
D000970:Antineoplastic Agents; C497483:CD44 protein, human; D018960:Hyaluronan Receptors; C486566:KIFC1 protein, human; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D043823:Taxoids; D000077143:Docetaxel; D016547:Kinesins
Cancer stem cells; Docetaxel; KIFC1; Prostate cancer