Mazumder Suman, Mitra Ghosh Taraswi, Mukherjee Ujjal K, Chakravarti Sayak, Amiri Farshad, Waliagha Razan S, Hemmati Farnaz, Mistriotis Panagiotis, Ahmed Salsabil, Elhussin Isra, Salam Ahmad-Bin, Dean-Colomb Windy, Yates Clayton, Arnold Robert D, Mitra Amit K
Department of Drug Discovery and Development, Harrison College of Pharmacy, Auburn University, Auburn, AL 36849, USA.
Center for Pharmacogenomics and Single-Cell Omics (AUPharmGx), Harrison College of Pharmacy, Auburn University, Auburn, AL 36849, USA.
Cancers (Basel). 2022 Dec 6;14(23):6009. doi: 10.3390/cancers14236009.
Metastatic prostate cancer/PCa is the second leading cause of cancer deaths in US men. Most early-stage PCa are dependent on overexpression of the androgen receptor (AR) and, therefore, androgen deprivation therapies/ADT-sensitive. However, eventual resistance to standard medical castration (AR-inhibitors) and secondary chemotherapies (taxanes) is nearly universal. Further, the presence of cancer stem-like cells (EMT/epithelial-to-mesenchymal transdifferentiation) and neuroendocrine PCa (NEPC) subtypes significantly contribute to aggressive/lethal/advanced variants of PCa (AVPC). In this study, we introduced a pharmacogenomics data-driven optimization-regularization-based computational prediction algorithm ("secDrugs") to predict novel drugs against lethal PCa. Integrating secDrug with single-cell RNA-sequencing/scRNAseq as a 'Double-Hit' drug screening tool, we demonstrated that single-cells representing drug-resistant and stem-cell-like cells showed high expression of the NAMPT pathway genes, indicating potential efficacy of the secDrug FK866 which targets NAMPT. Next, using several cell-based assays, we showed substantial impact of FK866 on clinically advanced PCa as a single agent and in combination with taxanes or AR-inhibitors. Bulk-RNAseq and scRNAseq revealed that, in addition to NAMPT inhibition, FK866 regulates tumor metastasis, cell migration, invasion, DNA repair machinery, redox homeostasis, autophagy, as well as cancer stemness-related genes, HES1 and CD44. Further, we combined a microfluidic chip-based cell migration assay with a traditional cell migration/'scratch' assay and demonstrated that FK866 reduces cancer cell invasion and motility, indicating abrogation of metastasis. Finally, using PCa patient datasets, we showed that FK866 is potentially capable of reversing the expression of several genes associated with biochemical recurrence, including IFITM3 and LTB4R. Thus, using FK866 as a proof-of-concept candidate for drug repurposing, we introduced a novel, universally applicable preclinical drug development pipeline to circumvent subclonal aggressiveness, drug resistance, and stemness in lethal PCa.
转移性前列腺癌(PCa)是美国男性癌症死亡的第二大主要原因。大多数早期PCa依赖雄激素受体(AR)的过表达,因此对雄激素剥夺疗法(ADT)敏感。然而,最终对标准药物去势(AR抑制剂)和二线化疗(紫杉烷类)产生耐药几乎是普遍现象。此外,癌症干细胞样细胞(EMT/上皮-间质转化)和神经内分泌PCa(NEPC)亚型的存在显著促成了PCa的侵袭性/致死性/晚期变体(AVPC)。在本研究中,我们引入了一种基于药物基因组学数据驱动的、优化正则化的计算预测算法(“secDrugs”)来预测针对致死性PCa的新型药物。将secDrug与单细胞RNA测序(scRNAseq)整合为一种“双重打击”药物筛选工具,我们证明代表耐药和干细胞样细胞的单细胞显示出NAMPT途径基因的高表达,这表明靶向NAMPT的secDrug FK866具有潜在疗效。接下来,通过几种基于细胞的检测方法,我们展示了FK866作为单一药物以及与紫杉烷类或AR抑制剂联合使用时,对临床晚期PCa有显著影响。批量RNA测序(Bulk-RNAseq)和scRNAseq显示,除了抑制NAMPT外,FK866还调节肿瘤转移、细胞迁移、侵袭、DNA修复机制、氧化还原稳态、自噬以及癌症干性相关基因HES1和CD44。此外,我们将基于微流控芯片的细胞迁移检测与传统细胞迁移/“划痕”检测相结合,证明FK866可降低癌细胞的侵袭和运动能力,表明其可消除转移。最后,利用PCa患者数据集,我们表明FK866有可能逆转与生化复发相关的几个基因的表达,包括IFITM3和LTB4R。因此,以FK866作为药物重新利用的概念验证候选药物,我们引入了一种新型的、普遍适用的临床前药物开发流程,以规避致死性PCa中的亚克隆侵袭性、耐药性和干性。