Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.
Department of Pathology, University of Chicago, Chicago, IL 60637, USA.
Cells. 2024 Sep 28;13(19):1622. doi: 10.3390/cells13191622.
Most patients with metastatic prostate cancer eventually develop resistance to primary androgen deprivation therapy. To identify predictive biomarker for Abiraterone acetate/prednisone resistance, we screened alternative splice variants between responders and non-responders from the PROMOTE clinical study and pinned down the most significant variant, CENPK-delta8. Through preclinical patient-derived mouse xenograft (PDX) and 3D organoids obtained from responders and non-responders, as well as in vitro models, aberrant CENPK-delta8 expression was determined to link to drug resistance via enhanced migration and proliferation. The FLNA and FLOT1 were observed to specifically bind to CENK-delta8 rather than wild-type CENPK, underscoring the role of CENPK-delta8 in cytoskeleton organization and cell migration. Our study, leveraging data from the PROMOTE study, TCGA, and TCGA SpliceReq databases, highlights the important function of alternative splice variants in drug response and their potential to be prognostic biomarkers for improving individual therapeutic outcomes in precision medicine.
大多数转移性前列腺癌患者最终会对主要的雄激素剥夺疗法产生耐药性。为了确定阿比特龙/泼尼松耐药的预测性生物标志物,我们从 PROMOTE 临床研究中筛选了应答者和无应答者之间的选择性剪接变体,并确定了最显著的变体 CENPK-delta8。通过来自应答者和无应答者的临床前患者来源的小鼠异种移植 (PDX) 和 3D 类器官以及体外模型,发现异常的 CENPK-delta8 表达通过增强迁移和增殖与耐药性相关。观察到 FLNA 和 FLOT1 特异性结合 CENK-delta8 而不是野生型 CENPK,这强调了 CENPK-delta8 在细胞骨架组织和细胞迁移中的作用。我们的研究利用了来自 PROMOTE 研究、TCGA 和 TCGA SpliceReq 数据库的数据,强调了选择性剪接变体在药物反应中的重要功能及其作为预后生物标志物的潜力,以改善精准医学中的个体治疗效果。