关键词：前列腺癌；凋亡；化疗；有丝分裂
摘 要：Docetaxel (DTX), a semi-synthetic analog of paclitaxel, has emerged as the standard of care for chemotherapy of hormone-resistant prostate cancer. Docetaxel confers its anti-neoplastic activity by inhibiting microtubule depolymerization, which leads to G2/M mitotic arrest and subsequent apoptosis (1). However, most patients treated with DTX ultimately develop resistance to the drug and succumb to the disease (2). Therefore, understanding the mechanisms underlying DTX resistance is a priority area in prostate cancer research. Previously, it was reported that CXCL12/CXCR4 signaling play an important role in microtubule organization in immune cells (3) and its inhibition induced mitotic catastrophe (G2/M arrest) in ovarian cancer cells (4). Based on these earlier observations, we hypothesized that CXCL12-CXCR4 signaling axis would promote docetaxel resistance by counteracting the microtubule stabilizing action of docetaxel.