Rationale: Docetaxel-mediated chemotherapy is the first-line standard approach and has been determined to show a survival advantage for metastatic castration-resistant prostate cancer (mCRPC) patients. However, a substantial proportion of patients eventually becomes refractory due to drug resistance. The detailed mechanisms remain unclear. We have previously reported that Prostate Leucine Zipper (PrLZ), a specific oncogene of prostate cancer (PCa), promotes PCa cell growth at the castration-resistant stage, thus suggesting a vital role of PrLZ in the progression of CRPC. In this study, we aimed to investigate the role of PrLZ in docetaxel resistance in PCa, focusing on PrLZ-regulating autophagy pathway.

中文翻译：

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PrLZ通过抑制LKB1 / AMPK介导的自噬增加前列腺癌多西他赛耐药性

基本原理：多西他赛介导的化学疗法是一线标准方法，已确定对转移性去势抵抗性前列腺癌（mCRPC）患者显示出生存优势。然而，由于抗药性，很大一部分患者最终变得难治。详细的机制仍不清楚。先前我们已经报道过前列腺亮氨酸拉链（PrLZ），一种前列腺癌（PCa）的特定致癌基因，在去势抵抗阶段促进PCa细胞的生长，因此表明PrLZ在CRPC的进展中起着至关重要的作用。在这项研究中，我们旨在研究PrLZ在PCa中对多西他赛耐药的作用，重点是PrLZ调节自噬途径。