**1. Introduction**

Prostate cancer (PCa) is the most prevalent cancer among men and the second leading cause of cancer-related death in developed countries [1]. Androgen deprivation therapy is initially effective for advanced PCa. However, most of these patients eventually progress to castration-resistant PCa (CRPC), which is a life-threatening disease [2,3]. Docetaxel (DTX) is the standard chemotherapy for CRPC [4]. However, nearly all patients who are treated with DTX become refractory. Therefore, clarifying new molecular mechanisms underlying DTX resistance is necessary to overcome DTX resistance in CRPC.

Increased centrosome number, called centrosome amplification (CA), is a hallmark of human cancer [5]. Recent reports have shown that CA correlates with aneuploidy and malignant behavior in some human cancers including uterine cervical cancer, breast cancer, and PCa [6,7]. Although aneuploidy might cause multipolar spindles and lead to apoptosis, cancer cells overcome these lethal effects of CA by using centrosome clustering. Centrosome clustering, defined as the reshaping of transient multipolar spindles into pseudo-bipolar structures, is a well-studied mechanism that allows cancer cells to avoid apoptosis [8,9]. Kinesin family member C1 (KIFC1) is a minus

end-directed motor protein that plays an essential role in centrosome clustering [10–12]. Several reports show that KIFC1 is upregulated and is involved in cancer progression in some cancers [13–15]. In addition, the overexpression of KIFC1 suppresses DTX-mediated apoptosis in breast cancer cells [16]. Previously, we showed that KIFC1 was associated with a poor prognosis after radical prostatectomy or after DTX treatment in PCa [17]. Additionally, knockdown of KIFC1 improved DTX sensitivity in LNCaP cells and DU145 cells. However, the role of KIFC1 in DTX resistance in PCa is not well known. In this study, we used DTX-resistant PCa cells from C4-2 cells and DU145 cells to analyze the involvement of KIFC1 in DTX resistance. We examined the expression and functional role of KIFC1 and analyzed the effect of KIFC1 knockdown on DTX resistance in DTX-resistant PCa cell lines. We also investigated the effect of the KIFC1 inhibitor CW069 in PCa cell lines.
