Despite recent advances in the treatment of metastatic prostate cancer (PCa), resistance development after taxane treatments is inevitable, necessitating effective options to combat drug resistance. Previous studies indicated antitumoral properties of the natural compound amygdalin. However, whether amygdalin acts on drug-resistant tumor cells remains questionable. An in vitro study was performed to investigate the influence of amygdalin (10 mg/mL) on the growth of a panel of therapy-naïve and docetaxel- or cabazitaxel-resistant PCa cell lines (PC3, DU145, and LNCaP cells). Tumor growth, proliferation, clonal growth, and cell cycle progression were investigated. The cell cycle regulating proteins (phospho)cdk1, (phospho)cdk2, cyclin A, cyclin B, p21, and p27 and the mammalian target of rapamycin (mTOR) pathway proteins (phospho)Akt, (phospho)Raptor, and (phospho)Rictor as well as integrin β1 and the cytoskeletal proteins vimentin, ezrin, talin, and cytokeratin 8/18 were assessed. Furthermore, chemotactic activity and adhesion to extracellular matrix components were analyzed. Amygdalin dose-dependently inhibited tumor growth and reduced tumor clones in all (parental and resistant) PCa cell lines, accompanied by a G0/G1 phase accumulation. Cell cycle regulating proteins were significantly altered by amygdalin. A moderate influence of amygdalin on tumor cell adhesion and chemotaxis was observed as well, paralleled by modifications of cytoskeletal proteins and the integrin β1 expression level. Amygdalin may, therefore, block tumor growth and disseminative characteristics of taxane-resistant PCa cells. Further studies are warranted to determine amygdalin's value as an antitumor drug.

中文翻译：

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苦杏仁苷在紫杉烷抗性前列腺癌细胞中发挥抗肿瘤活性。

尽管最近在治疗转移性前列腺癌 (PCa) 方面取得了进展，但紫杉烷治疗后耐药性的发展是不可避免的，因此需要有效的选择来对抗耐药性。先前的研究表明天然化合物苦杏仁苷的抗肿瘤特性。然而，苦杏仁苷是否作用于耐药肿瘤细胞仍然值得怀疑。进行了一项体外研究，以研究苦杏仁苷 (10 mg/mL) 对一组初治和多西他赛或卡巴他赛耐药的 PCa 细胞系（PC3、DU145 和 LNCaP 细胞）生长的影响。研究了肿瘤生长、增殖、克隆生长和细胞周期进程。细胞周期调节蛋白 (phospho)cdk1、(phospho)cdk2、cyclin A、cyclin B、p21 和 p27 以及哺乳动物雷帕霉素靶蛋白 (mTOR) 通路蛋白 (phospho)Akt，评估了（磷酸）Raptor 和（磷酸）Rictor 以及整合素 β1 和细胞骨架蛋白波形蛋白、埃兹蛋白、塔林和细胞角蛋白 8/18。此外，分析了趋化活性和对细胞外基质成分的粘附。苦杏仁苷剂量依赖性地抑制肿瘤生长并减少所有（亲本和抗性）PCa 细胞系中的肿瘤克隆，并伴有 G0/G1 期积累。苦杏仁苷显着改变了细胞周期调节蛋白。还观察到苦杏仁苷对肿瘤细胞粘附和趋化性的适度影响，与细胞骨架蛋白的修饰和整合素 β1 表达水平平行。因此，苦杏仁苷可能会阻止肿瘤生长和紫杉烷抗性 PCa 细胞的传播特征。需要进一步的研究来确定苦杏仁苷